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Hat-Wearing Patterns in Spectators Attending Baseball Games: A 10-Year Retrospective Comparison

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Hat-Wearing Patterns in Spectators Attending Baseball Games: A 10-Year Retrospective Comparison

Spectators at baseball games may be exposed to excess solar UV radiation (UVR), which has been linked to the development of both melanoma and nonmelanoma skin cancers.1,2 Although baseball hats traditionally are worn to demonstrate team support, they also may provide some sun protection for the head and face where skin cancers are commonly found.

The importance of protecting the skin from solar UVR has led to sun-protection programs and community education as well as efforts to evaluate the impact of these programs. Major League Baseball (MLB) has partnered with the American Academy of Dermatology since 1999 to promote the importance of sun protection and raise skin cancer awareness through its Play Sun Smart program.3 A study conducted 10 years ago (N=2030) evaluated hat use in spectators at MLB games and noted that less than half of all spectators in seating sections exposed to direct sunlight wore hats.4 The purpose of the current study was to evaluate how public education about sun protection has impacted the use of hats by spectators at MLB games in 2015 compared to the prior study in 2006.

Methods

Data were collected during a 3-game series (2 day games, 1 night game) in August 2015 in New York, New York. During one of the day games, 18,000 fans received a free wide-brimmed hat. High-resolution digital photographs of seating sections were obtained using a camera with a 300-mm lens. Using the same methodology as the prior study,4 sunny and shaded seating sections were photographed during all 3 games (Figure). Photographs of each section were analyzed by an independent reviewer using a high-resolution computer screen. Spectators wearing head coverings—baseball hats, visors, or hats with circumferential brims—were defined as using hats. The number of spectators wearing hats versus not wearing hats was recorded for all identical sections of interest. Bleacher seating was analyzed separately, as spectators presumably knew in advance of the continuous direct sun exposure during day games, and a subset of young children in the bleachers (<10 years of age) also was assessed. A continuously sunny section also was evaluated at the second and sixth innings to see if hats were presumably purchased during exposure. Statistical significance was determined using χ2 tests with P<.05 indicating statistical significance.

Representative photographs of spectators at a daytime baseball game sitting in adjacent sunny and shaded sections (A) and spectators sitting in the bleachers during a day game with a free hat giveaway (B).

Results

This analysis consisted of 3539 spectators. In both the sunny and shaded sections of a day game, there were more spectators wearing hats (49% and 37%, respectively)(P<.001) than in the same sections at night games (35% and 29%, respectively)(Table 1). During the day game, more spectators wore hats in the sunny section than in the adjacent shaded section (49% vs 37%; P<.001). Analysis of the same 2 sections during the night game revealed no significant differences.

Spectators sitting in the bleachers during a day game who presumably knew to anticipate direct sun exposure showed no significant differences in hat-wearing patterns versus the sunny section (44% vs 49%) but were more likely to wear hats compared to those sitting in the bleachers at the night game (44% vs 33%)(P<.001)(Table 1). There was no significant difference in the number of hats worn by spectators in the sunny section in the second inning (43%) versus the same section after continuous sun exposure at the sixth inning (44%)(Table 2). Significantly more children seated in the bleachers during the day game wore hats compared to adults in the same section (64% vs 42%; P<.001)(Table 3). During the hat giveaway day, significantly more spectators wore hats (the majority of which were the free giveaway hats) across all sections studied (P<.001)(Table 4).

 

 

Comment

More than 23 million spectators attended daytime MLB games in 2015, with millions more attending minor league and amateur events.5Although sun-protection messages tend to be well understood and received by society, many choose to ignore them.6

In partnership with the American Academy of Dermatology, the MLB’s Play Sun Smart program has promoted UVR risk awareness at sporting events since 1999.3 Those affiliated with MLB teams also receive annual skin cancer screenings in conjunction with a public education effort in May of each season. However, despite the years of sun-protection education, our study found that less than half of attendees wore hats for UVR protection. In fact, there were no significant differences noted across all of the hat-wearing parameters studied (day vs night game, sunny vs shaded section, sunny section over course of game) between the current study compared to the results from 10 years prior4 (Tables 1 and 2). For spectators in the bleacher section, even presumably knowing in advance that seating would be in the sun did not significantly increase hat-wearing behavior. Although skin cancer rates continue to rise, hat-wearing trends remain stable, revealing a concerning trend.

Increased availability of sunscreen has led to improved sun-protective behaviors in many populations.7 In our study, the free hat giveaway had the greatest impact on hat wearing, which suggests that improved availability and access to hats can lead to an important opportunity for sun-protection programs to partner with hat manufacturers to augment their use and protective impact.

Sun avoidance during childhood and adolescence has been shown to decrease the risk for melanoma.1 Young children had the highest rate of hat usage in the current study, possibly due to parental example or dictates. Research has shown the importance of role models in promoting sun safety to young children,8,9 so perhaps use of hats by parents or MLB players contributed to the hat-wearing behavior observed in this subpopulation.

Given the limited change observed in hat-wearing behaviors over the last decade, a knowledge and behavioral gap appears to exist that may be able to be exploited to enhance future sun protection. Also, based on our findings, the MLB and other sun-protection education campaigns may wish to augment their UVR protective messages by offering hat giveaways, which appear to have a notable impact.

Acknowledgment

The authors thank Jessie Skapik, BS (New York, New York), for her independent review of the spectator photographs.

References

References

1. Rigel DS. Cutaneous ultraviolet exposure and its relationship to the development of skin cancer. J Am Acad Dermatol. 2008;58(5, suppl 2):S129-S132.

2. Lim HW, James WD, Rigel DS, et al. Adverse effects of ultraviolet radiation from the use of indoor tanning equipment: time to ban the tan. J Am Acad Dermatol. 2011;64:893-902.

3. Play Sun Smart. American Academy of Dermatology website. https://www.aad.org/public/spot-skin-cancer/programs/play-sun-smart. Accessed August 25, 2016.

4. Rigel AS, Lebwohl MG. Hat-wearing patterns in persons attending baseball games. J Am Acad Dermatol. 2006;54:918-919.

5. MLB attendance report - 2016. ESPN website. www.espn.go.com/mlb/attendance. Accessed May 20, 2016.

6. Turner D, Harrison SL, Buettner P, et al. Does being a “SunSmart School” influence hat-wearing compliance? an ecological study of hat-wearing rates at Australian primary schools in a region of high sun exposure [published online December 29, 2013]. Prev Med. 2014;60:107-114.

7. Dubas LE, Adams BB. Sunscreen use and availability among female collegiate athletes [published online February 3, 2012]. J Am Acad Dermatol. 2012;67:876.e1-876.e6.

8. O’Riodran DL, Geller AC, Brooks DR, et al. Sunburn reduction through parental role modeling and sunscreen vigilance. J Pediatr. 2003;142:67-72.

9. Turrisi R, Hillhouse J, Heavin S, et al. Examination of the short-term efficacy of a parent-based intervention to prevent skin cancer. J Behav Med. 2004;27:393-412.

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Dr. Farberg is from the Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, New York. Mr. Donohue is from the New York Yankees, New York. Dr. Rigel is from the Ronald O. Perelman Department of Dermatology, New York University School of Medicine, New York.

The authors report no conflict of interest.

Correspondence: Darrell S. Rigel, MD, MS, Ronald O. Perelman Department of Dermatology, New York University School of Medicine, 35 E 35th St, Ste 208, New York, NY 10016 ([email protected]).

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Dr. Farberg is from the Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, New York. Mr. Donohue is from the New York Yankees, New York. Dr. Rigel is from the Ronald O. Perelman Department of Dermatology, New York University School of Medicine, New York.

The authors report no conflict of interest.

Correspondence: Darrell S. Rigel, MD, MS, Ronald O. Perelman Department of Dermatology, New York University School of Medicine, 35 E 35th St, Ste 208, New York, NY 10016 ([email protected]).

Author and Disclosure Information

Dr. Farberg is from the Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, New York. Mr. Donohue is from the New York Yankees, New York. Dr. Rigel is from the Ronald O. Perelman Department of Dermatology, New York University School of Medicine, New York.

The authors report no conflict of interest.

Correspondence: Darrell S. Rigel, MD, MS, Ronald O. Perelman Department of Dermatology, New York University School of Medicine, 35 E 35th St, Ste 208, New York, NY 10016 ([email protected]).

Article PDF
Article PDF

Spectators at baseball games may be exposed to excess solar UV radiation (UVR), which has been linked to the development of both melanoma and nonmelanoma skin cancers.1,2 Although baseball hats traditionally are worn to demonstrate team support, they also may provide some sun protection for the head and face where skin cancers are commonly found.

The importance of protecting the skin from solar UVR has led to sun-protection programs and community education as well as efforts to evaluate the impact of these programs. Major League Baseball (MLB) has partnered with the American Academy of Dermatology since 1999 to promote the importance of sun protection and raise skin cancer awareness through its Play Sun Smart program.3 A study conducted 10 years ago (N=2030) evaluated hat use in spectators at MLB games and noted that less than half of all spectators in seating sections exposed to direct sunlight wore hats.4 The purpose of the current study was to evaluate how public education about sun protection has impacted the use of hats by spectators at MLB games in 2015 compared to the prior study in 2006.

Methods

Data were collected during a 3-game series (2 day games, 1 night game) in August 2015 in New York, New York. During one of the day games, 18,000 fans received a free wide-brimmed hat. High-resolution digital photographs of seating sections were obtained using a camera with a 300-mm lens. Using the same methodology as the prior study,4 sunny and shaded seating sections were photographed during all 3 games (Figure). Photographs of each section were analyzed by an independent reviewer using a high-resolution computer screen. Spectators wearing head coverings—baseball hats, visors, or hats with circumferential brims—were defined as using hats. The number of spectators wearing hats versus not wearing hats was recorded for all identical sections of interest. Bleacher seating was analyzed separately, as spectators presumably knew in advance of the continuous direct sun exposure during day games, and a subset of young children in the bleachers (<10 years of age) also was assessed. A continuously sunny section also was evaluated at the second and sixth innings to see if hats were presumably purchased during exposure. Statistical significance was determined using χ2 tests with P<.05 indicating statistical significance.

Representative photographs of spectators at a daytime baseball game sitting in adjacent sunny and shaded sections (A) and spectators sitting in the bleachers during a day game with a free hat giveaway (B).

Results

This analysis consisted of 3539 spectators. In both the sunny and shaded sections of a day game, there were more spectators wearing hats (49% and 37%, respectively)(P<.001) than in the same sections at night games (35% and 29%, respectively)(Table 1). During the day game, more spectators wore hats in the sunny section than in the adjacent shaded section (49% vs 37%; P<.001). Analysis of the same 2 sections during the night game revealed no significant differences.

Spectators sitting in the bleachers during a day game who presumably knew to anticipate direct sun exposure showed no significant differences in hat-wearing patterns versus the sunny section (44% vs 49%) but were more likely to wear hats compared to those sitting in the bleachers at the night game (44% vs 33%)(P<.001)(Table 1). There was no significant difference in the number of hats worn by spectators in the sunny section in the second inning (43%) versus the same section after continuous sun exposure at the sixth inning (44%)(Table 2). Significantly more children seated in the bleachers during the day game wore hats compared to adults in the same section (64% vs 42%; P<.001)(Table 3). During the hat giveaway day, significantly more spectators wore hats (the majority of which were the free giveaway hats) across all sections studied (P<.001)(Table 4).

 

 

Comment

More than 23 million spectators attended daytime MLB games in 2015, with millions more attending minor league and amateur events.5Although sun-protection messages tend to be well understood and received by society, many choose to ignore them.6

In partnership with the American Academy of Dermatology, the MLB’s Play Sun Smart program has promoted UVR risk awareness at sporting events since 1999.3 Those affiliated with MLB teams also receive annual skin cancer screenings in conjunction with a public education effort in May of each season. However, despite the years of sun-protection education, our study found that less than half of attendees wore hats for UVR protection. In fact, there were no significant differences noted across all of the hat-wearing parameters studied (day vs night game, sunny vs shaded section, sunny section over course of game) between the current study compared to the results from 10 years prior4 (Tables 1 and 2). For spectators in the bleacher section, even presumably knowing in advance that seating would be in the sun did not significantly increase hat-wearing behavior. Although skin cancer rates continue to rise, hat-wearing trends remain stable, revealing a concerning trend.

Increased availability of sunscreen has led to improved sun-protective behaviors in many populations.7 In our study, the free hat giveaway had the greatest impact on hat wearing, which suggests that improved availability and access to hats can lead to an important opportunity for sun-protection programs to partner with hat manufacturers to augment their use and protective impact.

Sun avoidance during childhood and adolescence has been shown to decrease the risk for melanoma.1 Young children had the highest rate of hat usage in the current study, possibly due to parental example or dictates. Research has shown the importance of role models in promoting sun safety to young children,8,9 so perhaps use of hats by parents or MLB players contributed to the hat-wearing behavior observed in this subpopulation.

Given the limited change observed in hat-wearing behaviors over the last decade, a knowledge and behavioral gap appears to exist that may be able to be exploited to enhance future sun protection. Also, based on our findings, the MLB and other sun-protection education campaigns may wish to augment their UVR protective messages by offering hat giveaways, which appear to have a notable impact.

Acknowledgment

The authors thank Jessie Skapik, BS (New York, New York), for her independent review of the spectator photographs.

Spectators at baseball games may be exposed to excess solar UV radiation (UVR), which has been linked to the development of both melanoma and nonmelanoma skin cancers.1,2 Although baseball hats traditionally are worn to demonstrate team support, they also may provide some sun protection for the head and face where skin cancers are commonly found.

The importance of protecting the skin from solar UVR has led to sun-protection programs and community education as well as efforts to evaluate the impact of these programs. Major League Baseball (MLB) has partnered with the American Academy of Dermatology since 1999 to promote the importance of sun protection and raise skin cancer awareness through its Play Sun Smart program.3 A study conducted 10 years ago (N=2030) evaluated hat use in spectators at MLB games and noted that less than half of all spectators in seating sections exposed to direct sunlight wore hats.4 The purpose of the current study was to evaluate how public education about sun protection has impacted the use of hats by spectators at MLB games in 2015 compared to the prior study in 2006.

Methods

Data were collected during a 3-game series (2 day games, 1 night game) in August 2015 in New York, New York. During one of the day games, 18,000 fans received a free wide-brimmed hat. High-resolution digital photographs of seating sections were obtained using a camera with a 300-mm lens. Using the same methodology as the prior study,4 sunny and shaded seating sections were photographed during all 3 games (Figure). Photographs of each section were analyzed by an independent reviewer using a high-resolution computer screen. Spectators wearing head coverings—baseball hats, visors, or hats with circumferential brims—were defined as using hats. The number of spectators wearing hats versus not wearing hats was recorded for all identical sections of interest. Bleacher seating was analyzed separately, as spectators presumably knew in advance of the continuous direct sun exposure during day games, and a subset of young children in the bleachers (<10 years of age) also was assessed. A continuously sunny section also was evaluated at the second and sixth innings to see if hats were presumably purchased during exposure. Statistical significance was determined using χ2 tests with P<.05 indicating statistical significance.

Representative photographs of spectators at a daytime baseball game sitting in adjacent sunny and shaded sections (A) and spectators sitting in the bleachers during a day game with a free hat giveaway (B).

Results

This analysis consisted of 3539 spectators. In both the sunny and shaded sections of a day game, there were more spectators wearing hats (49% and 37%, respectively)(P<.001) than in the same sections at night games (35% and 29%, respectively)(Table 1). During the day game, more spectators wore hats in the sunny section than in the adjacent shaded section (49% vs 37%; P<.001). Analysis of the same 2 sections during the night game revealed no significant differences.

Spectators sitting in the bleachers during a day game who presumably knew to anticipate direct sun exposure showed no significant differences in hat-wearing patterns versus the sunny section (44% vs 49%) but were more likely to wear hats compared to those sitting in the bleachers at the night game (44% vs 33%)(P<.001)(Table 1). There was no significant difference in the number of hats worn by spectators in the sunny section in the second inning (43%) versus the same section after continuous sun exposure at the sixth inning (44%)(Table 2). Significantly more children seated in the bleachers during the day game wore hats compared to adults in the same section (64% vs 42%; P<.001)(Table 3). During the hat giveaway day, significantly more spectators wore hats (the majority of which were the free giveaway hats) across all sections studied (P<.001)(Table 4).

 

 

Comment

More than 23 million spectators attended daytime MLB games in 2015, with millions more attending minor league and amateur events.5Although sun-protection messages tend to be well understood and received by society, many choose to ignore them.6

In partnership with the American Academy of Dermatology, the MLB’s Play Sun Smart program has promoted UVR risk awareness at sporting events since 1999.3 Those affiliated with MLB teams also receive annual skin cancer screenings in conjunction with a public education effort in May of each season. However, despite the years of sun-protection education, our study found that less than half of attendees wore hats for UVR protection. In fact, there were no significant differences noted across all of the hat-wearing parameters studied (day vs night game, sunny vs shaded section, sunny section over course of game) between the current study compared to the results from 10 years prior4 (Tables 1 and 2). For spectators in the bleacher section, even presumably knowing in advance that seating would be in the sun did not significantly increase hat-wearing behavior. Although skin cancer rates continue to rise, hat-wearing trends remain stable, revealing a concerning trend.

Increased availability of sunscreen has led to improved sun-protective behaviors in many populations.7 In our study, the free hat giveaway had the greatest impact on hat wearing, which suggests that improved availability and access to hats can lead to an important opportunity for sun-protection programs to partner with hat manufacturers to augment their use and protective impact.

Sun avoidance during childhood and adolescence has been shown to decrease the risk for melanoma.1 Young children had the highest rate of hat usage in the current study, possibly due to parental example or dictates. Research has shown the importance of role models in promoting sun safety to young children,8,9 so perhaps use of hats by parents or MLB players contributed to the hat-wearing behavior observed in this subpopulation.

Given the limited change observed in hat-wearing behaviors over the last decade, a knowledge and behavioral gap appears to exist that may be able to be exploited to enhance future sun protection. Also, based on our findings, the MLB and other sun-protection education campaigns may wish to augment their UVR protective messages by offering hat giveaways, which appear to have a notable impact.

Acknowledgment

The authors thank Jessie Skapik, BS (New York, New York), for her independent review of the spectator photographs.

References

References

1. Rigel DS. Cutaneous ultraviolet exposure and its relationship to the development of skin cancer. J Am Acad Dermatol. 2008;58(5, suppl 2):S129-S132.

2. Lim HW, James WD, Rigel DS, et al. Adverse effects of ultraviolet radiation from the use of indoor tanning equipment: time to ban the tan. J Am Acad Dermatol. 2011;64:893-902.

3. Play Sun Smart. American Academy of Dermatology website. https://www.aad.org/public/spot-skin-cancer/programs/play-sun-smart. Accessed August 25, 2016.

4. Rigel AS, Lebwohl MG. Hat-wearing patterns in persons attending baseball games. J Am Acad Dermatol. 2006;54:918-919.

5. MLB attendance report - 2016. ESPN website. www.espn.go.com/mlb/attendance. Accessed May 20, 2016.

6. Turner D, Harrison SL, Buettner P, et al. Does being a “SunSmart School” influence hat-wearing compliance? an ecological study of hat-wearing rates at Australian primary schools in a region of high sun exposure [published online December 29, 2013]. Prev Med. 2014;60:107-114.

7. Dubas LE, Adams BB. Sunscreen use and availability among female collegiate athletes [published online February 3, 2012]. J Am Acad Dermatol. 2012;67:876.e1-876.e6.

8. O’Riodran DL, Geller AC, Brooks DR, et al. Sunburn reduction through parental role modeling and sunscreen vigilance. J Pediatr. 2003;142:67-72.

9. Turrisi R, Hillhouse J, Heavin S, et al. Examination of the short-term efficacy of a parent-based intervention to prevent skin cancer. J Behav Med. 2004;27:393-412.

References

References

1. Rigel DS. Cutaneous ultraviolet exposure and its relationship to the development of skin cancer. J Am Acad Dermatol. 2008;58(5, suppl 2):S129-S132.

2. Lim HW, James WD, Rigel DS, et al. Adverse effects of ultraviolet radiation from the use of indoor tanning equipment: time to ban the tan. J Am Acad Dermatol. 2011;64:893-902.

3. Play Sun Smart. American Academy of Dermatology website. https://www.aad.org/public/spot-skin-cancer/programs/play-sun-smart. Accessed August 25, 2016.

4. Rigel AS, Lebwohl MG. Hat-wearing patterns in persons attending baseball games. J Am Acad Dermatol. 2006;54:918-919.

5. MLB attendance report - 2016. ESPN website. www.espn.go.com/mlb/attendance. Accessed May 20, 2016.

6. Turner D, Harrison SL, Buettner P, et al. Does being a “SunSmart School” influence hat-wearing compliance? an ecological study of hat-wearing rates at Australian primary schools in a region of high sun exposure [published online December 29, 2013]. Prev Med. 2014;60:107-114.

7. Dubas LE, Adams BB. Sunscreen use and availability among female collegiate athletes [published online February 3, 2012]. J Am Acad Dermatol. 2012;67:876.e1-876.e6.

8. O’Riodran DL, Geller AC, Brooks DR, et al. Sunburn reduction through parental role modeling and sunscreen vigilance. J Pediatr. 2003;142:67-72.

9. Turrisi R, Hillhouse J, Heavin S, et al. Examination of the short-term efficacy of a parent-based intervention to prevent skin cancer. J Behav Med. 2004;27:393-412.

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  • With less than half of attendees wearing hats to Major League Baseball games, there has been limited change in hat-wearing behavior over the last decade, possibly due to a knowledge or behavioral gap.
  • Improved availability and access to hats can lead to improved sun-protective behaviors.
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Nevus Spilus: Is the Presence of Hair Associated With an Increased Risk for Melanoma?

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Nevus Spilus: Is the Presence of Hair Associated With an Increased Risk for Melanoma?

The term nevus spilus (NS), also known as speckled lentiginous nevus, was first used in the 19th century to describe lesions with background café au lait–like lentiginous melanocytic hyperplasia speckled with small, 1- to 3-mm, darker foci. The dark spots reflect lentigines; junctional, compound, and intradermal nevus cell nests; and more rarely Spitz and blue nevi. Both macular and papular subtypes have been described.1 This birthmark is quite common, occurring in 1.3% to 2.3% of the adult population worldwide.2 Hypertrichosis has been described in NS.3-9 Two subsequent cases of malignant melanoma in hairy NS suggested that lesions may be particularly prone to malignant degeneration.4,8 We report an additional case of hairy NS that was not associated with melanoma and consider whether dermatologists should warn their patients about this association.

Case Report

A 26-year-old woman presented with a stable 7×8-cm, tan-brown, macular, pigmented birthmark studded with darker 1- to 2-mm, irregular, brown-black and blue, confettilike macules on the left proximal lateral thigh that had been present since birth (Figure 1). Dark terminal hairs were present, arising from both the darker and lighter pigmented areas but not the surrounding normal skin.

Figure 1. A 7×8-cm tan-brown macule studded with darker macules and slightly raised papules on the thigh that was later diagnosed as nevus spilus. Terminal hairs were present.

A 4-mm punch biopsy from one of the dark blue macules demonstrated uniform lentiginous melanocytic hyperplasia and nevus cell nests adjacent to the sweat glands extending into the mid dermis (Figure 2). No clinical evidence of malignant degeneration was present.

Figure 2. Histopathology revealed lentiginous melanocytic hyperplasia, most prominent at the tips of rete pegs, correlating clinically with the café au lait background coloration, and nevus cells adjacent to the sweat glands extending into the mid dermis, correlating with the blue-black papules (A and B)(H&E, original magnifications ×200 and ×100).

Comment

The risk for melanoma is increased in classic nonspeckled congenital nevi and the risk correlates with the size of the lesion and most probably the number of nevus cells in the lesion that increase the risk for a random mutation.8,10,11 It is likely that NS with or without hair presages a small increased risk for melanoma,6,9,12 which is not surprising because NS is a subtype of congenital melanocytic nevus (CMN), a condition that is present at birth and results from a proliferation of melanocytes.6 Nevus spilus, however, appears to have a notably lower risk for malignant degeneration than other classic CMN of the same size. The following support for this hypothesis is offered: First, CMN have nevus cells broadly filling the dermis that extend more deeply into the dermis than NS (Figure 2A).10 In our estimation, CMN have at least 100 times the number of nevus cells per square centimeter compared to NS. The potential for malignant degeneration of any one melanocyte is greater when more are present. Second, although some NS lesions evolve, classic CMN are universally more proliferative than NS.10,13 The involved skin in CMN thickens over time with increased numbers of melanocytes and marked overgrowth of adjacent tissue. Melanocytes in a proliferative phase may be more likely to undergo malignant degeneration.10

 

 

A PubMed search of articles indexed for MEDLINE using the search term nevus spilus and melanoma yielded 2 cases4,8 of melanoma arising among 15 cases of hairy NS in the literature, which led to the suggestion that the presence of hair could be associated with an increased risk for malignant degeneration in NS (Table). This apparent high incidence of melanoma most likely reflects referral/publication bias rather than a statistically significant association. In fact, the clinical lesion most clinically similar to hairy NS is Becker nevus, with tan macules demonstrating lentiginous melanocytic hyperplasia associated with numerous coarse terminal hairs. There is no indication that Becker nevi have a considerable premalignant potential, though one case of melanoma arising in a Becker nevus has been reported.9 There is no evidence to suggest that classic CMN with hypertrichosis has a greater premalignant potential than similar lesions without hypertrichosis.


We noticed the presence of hair in our patient’s lesion only after reports in the literature caused us to look for this phenomenon.9 This occurrence may actually be quite common. We do not recommend prophylactic excision of NS and believe the risk for malignant degeneration is low in NS with or without hair, though larger NS (>4 cm), especially giant, zosteriform, or segmental lesions, may have a greater risk.1,6,9,10 It is prudent for physicians to carefully examine NS and sample suspicious foci, especially when patients describe a lesion as changing.

References
  1. Vidaurri-de la Cruz H, Happle R. Two distinct types of speckled lentiginous nevi characterized by macular versus papular speckles. Dermatology. 2006;212:53-58.
  2. Ly L, Christie M, Swain S, et al. Melanoma(s) arising in large segmental speckled lentiginous nevi: a case series. J Am Acad Dermatol. 2011;64:1190-1193.
  3. Prose NS, Heilman E, Felman YM, et al. Multiple benign juvenile melanoma. J Am Acad Dermatol. 1983;9:236-242.
  4. Grinspan D, Casala A, Abulafia J, et al. Melanoma on dysplastic nevus spilus. Int J Dermatol. 1997;36:499-502 .
  5. Langenbach N, Pfau A, Landthaler M, et al. Naevi spili, café-au-lait spots and melanocytic naevi aggregated alongside Blaschko’s lines, with a review of segmental melanocytic lesions. Acta Derm Venereol. 1998;78:378-380.
  6. Schaffer JV, Orlow SJ, Lazova R, et al. Speckled lentiginous nevus: within the spectrum of congenital melanocytic nevi. Arch Dermatol. 2001;137:172-178.
  7. Saraswat A, Dogra S, Bansali A, et al. Phakomatosis pigmentokeratotica associated with hypophosphataemic vitamin D–resistant rickets: improvement in phosphate homeostasis after partial laser ablation. Br J Dermatol. 2003;148:1074-1076.
  8. Zeren-Bilgin i, Gür S, Aydın O, et al. Melanoma arising in a hairy nevus spilus. Int J Dermatol. 2006;45:1362-1364.
  9. Singh S, Jain N, Khanna N, et al. Hairy nevus spilus: a case series. Pediatr Dermatol. 2013;30:100-104.
  10. Price HN, Schaffer JV. Congenital melanocytic nevi—when to worry and how to treat: facts and controversies. Clin Dermatol. 2010;28:293-302.
  11. Alikhan Ali, Ibrahimi OA, Eisen DB. Congenital melanocytic nevi: where are we now? J Am Acad Dermatol. 2012;67:495.e1-495.e17.
  12. Haenssle HA, Kaune KM, Buhl T, et al. Melanoma arising in segmental nevus spilus: detection by sequential digital dermatoscopy. J Am Acad Dermatol. 2009;61:337-341.
  13. Cohen LM. Nevus spilus: congenital or acquired? Arch Dermatol. 2001;137:215-216.
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Drs. Gathings, Reddy, and Brodell are from the Department of Dermatology, University of Mississippi Medical Center, Jackson. Dr. Bhatia is from Northwestern University Feinberg School of Medicine, Chicago, Illinois.

The authors report no conflict of interest.

Correspondence: Robert T. Brodell, MD, Division of Dermatology, University of Mississippi Medical Center, 2500 N State St, Jackson, MS 39216 ([email protected]).

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Drs. Gathings, Reddy, and Brodell are from the Department of Dermatology, University of Mississippi Medical Center, Jackson. Dr. Bhatia is from Northwestern University Feinberg School of Medicine, Chicago, Illinois.

The authors report no conflict of interest.

Correspondence: Robert T. Brodell, MD, Division of Dermatology, University of Mississippi Medical Center, 2500 N State St, Jackson, MS 39216 ([email protected]).

Author and Disclosure Information

Drs. Gathings, Reddy, and Brodell are from the Department of Dermatology, University of Mississippi Medical Center, Jackson. Dr. Bhatia is from Northwestern University Feinberg School of Medicine, Chicago, Illinois.

The authors report no conflict of interest.

Correspondence: Robert T. Brodell, MD, Division of Dermatology, University of Mississippi Medical Center, 2500 N State St, Jackson, MS 39216 ([email protected]).

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The term nevus spilus (NS), also known as speckled lentiginous nevus, was first used in the 19th century to describe lesions with background café au lait–like lentiginous melanocytic hyperplasia speckled with small, 1- to 3-mm, darker foci. The dark spots reflect lentigines; junctional, compound, and intradermal nevus cell nests; and more rarely Spitz and blue nevi. Both macular and papular subtypes have been described.1 This birthmark is quite common, occurring in 1.3% to 2.3% of the adult population worldwide.2 Hypertrichosis has been described in NS.3-9 Two subsequent cases of malignant melanoma in hairy NS suggested that lesions may be particularly prone to malignant degeneration.4,8 We report an additional case of hairy NS that was not associated with melanoma and consider whether dermatologists should warn their patients about this association.

Case Report

A 26-year-old woman presented with a stable 7×8-cm, tan-brown, macular, pigmented birthmark studded with darker 1- to 2-mm, irregular, brown-black and blue, confettilike macules on the left proximal lateral thigh that had been present since birth (Figure 1). Dark terminal hairs were present, arising from both the darker and lighter pigmented areas but not the surrounding normal skin.

Figure 1. A 7×8-cm tan-brown macule studded with darker macules and slightly raised papules on the thigh that was later diagnosed as nevus spilus. Terminal hairs were present.

A 4-mm punch biopsy from one of the dark blue macules demonstrated uniform lentiginous melanocytic hyperplasia and nevus cell nests adjacent to the sweat glands extending into the mid dermis (Figure 2). No clinical evidence of malignant degeneration was present.

Figure 2. Histopathology revealed lentiginous melanocytic hyperplasia, most prominent at the tips of rete pegs, correlating clinically with the café au lait background coloration, and nevus cells adjacent to the sweat glands extending into the mid dermis, correlating with the blue-black papules (A and B)(H&E, original magnifications ×200 and ×100).

Comment

The risk for melanoma is increased in classic nonspeckled congenital nevi and the risk correlates with the size of the lesion and most probably the number of nevus cells in the lesion that increase the risk for a random mutation.8,10,11 It is likely that NS with or without hair presages a small increased risk for melanoma,6,9,12 which is not surprising because NS is a subtype of congenital melanocytic nevus (CMN), a condition that is present at birth and results from a proliferation of melanocytes.6 Nevus spilus, however, appears to have a notably lower risk for malignant degeneration than other classic CMN of the same size. The following support for this hypothesis is offered: First, CMN have nevus cells broadly filling the dermis that extend more deeply into the dermis than NS (Figure 2A).10 In our estimation, CMN have at least 100 times the number of nevus cells per square centimeter compared to NS. The potential for malignant degeneration of any one melanocyte is greater when more are present. Second, although some NS lesions evolve, classic CMN are universally more proliferative than NS.10,13 The involved skin in CMN thickens over time with increased numbers of melanocytes and marked overgrowth of adjacent tissue. Melanocytes in a proliferative phase may be more likely to undergo malignant degeneration.10

 

 

A PubMed search of articles indexed for MEDLINE using the search term nevus spilus and melanoma yielded 2 cases4,8 of melanoma arising among 15 cases of hairy NS in the literature, which led to the suggestion that the presence of hair could be associated with an increased risk for malignant degeneration in NS (Table). This apparent high incidence of melanoma most likely reflects referral/publication bias rather than a statistically significant association. In fact, the clinical lesion most clinically similar to hairy NS is Becker nevus, with tan macules demonstrating lentiginous melanocytic hyperplasia associated with numerous coarse terminal hairs. There is no indication that Becker nevi have a considerable premalignant potential, though one case of melanoma arising in a Becker nevus has been reported.9 There is no evidence to suggest that classic CMN with hypertrichosis has a greater premalignant potential than similar lesions without hypertrichosis.


We noticed the presence of hair in our patient’s lesion only after reports in the literature caused us to look for this phenomenon.9 This occurrence may actually be quite common. We do not recommend prophylactic excision of NS and believe the risk for malignant degeneration is low in NS with or without hair, though larger NS (>4 cm), especially giant, zosteriform, or segmental lesions, may have a greater risk.1,6,9,10 It is prudent for physicians to carefully examine NS and sample suspicious foci, especially when patients describe a lesion as changing.

The term nevus spilus (NS), also known as speckled lentiginous nevus, was first used in the 19th century to describe lesions with background café au lait–like lentiginous melanocytic hyperplasia speckled with small, 1- to 3-mm, darker foci. The dark spots reflect lentigines; junctional, compound, and intradermal nevus cell nests; and more rarely Spitz and blue nevi. Both macular and papular subtypes have been described.1 This birthmark is quite common, occurring in 1.3% to 2.3% of the adult population worldwide.2 Hypertrichosis has been described in NS.3-9 Two subsequent cases of malignant melanoma in hairy NS suggested that lesions may be particularly prone to malignant degeneration.4,8 We report an additional case of hairy NS that was not associated with melanoma and consider whether dermatologists should warn their patients about this association.

Case Report

A 26-year-old woman presented with a stable 7×8-cm, tan-brown, macular, pigmented birthmark studded with darker 1- to 2-mm, irregular, brown-black and blue, confettilike macules on the left proximal lateral thigh that had been present since birth (Figure 1). Dark terminal hairs were present, arising from both the darker and lighter pigmented areas but not the surrounding normal skin.

Figure 1. A 7×8-cm tan-brown macule studded with darker macules and slightly raised papules on the thigh that was later diagnosed as nevus spilus. Terminal hairs were present.

A 4-mm punch biopsy from one of the dark blue macules demonstrated uniform lentiginous melanocytic hyperplasia and nevus cell nests adjacent to the sweat glands extending into the mid dermis (Figure 2). No clinical evidence of malignant degeneration was present.

Figure 2. Histopathology revealed lentiginous melanocytic hyperplasia, most prominent at the tips of rete pegs, correlating clinically with the café au lait background coloration, and nevus cells adjacent to the sweat glands extending into the mid dermis, correlating with the blue-black papules (A and B)(H&E, original magnifications ×200 and ×100).

Comment

The risk for melanoma is increased in classic nonspeckled congenital nevi and the risk correlates with the size of the lesion and most probably the number of nevus cells in the lesion that increase the risk for a random mutation.8,10,11 It is likely that NS with or without hair presages a small increased risk for melanoma,6,9,12 which is not surprising because NS is a subtype of congenital melanocytic nevus (CMN), a condition that is present at birth and results from a proliferation of melanocytes.6 Nevus spilus, however, appears to have a notably lower risk for malignant degeneration than other classic CMN of the same size. The following support for this hypothesis is offered: First, CMN have nevus cells broadly filling the dermis that extend more deeply into the dermis than NS (Figure 2A).10 In our estimation, CMN have at least 100 times the number of nevus cells per square centimeter compared to NS. The potential for malignant degeneration of any one melanocyte is greater when more are present. Second, although some NS lesions evolve, classic CMN are universally more proliferative than NS.10,13 The involved skin in CMN thickens over time with increased numbers of melanocytes and marked overgrowth of adjacent tissue. Melanocytes in a proliferative phase may be more likely to undergo malignant degeneration.10

 

 

A PubMed search of articles indexed for MEDLINE using the search term nevus spilus and melanoma yielded 2 cases4,8 of melanoma arising among 15 cases of hairy NS in the literature, which led to the suggestion that the presence of hair could be associated with an increased risk for malignant degeneration in NS (Table). This apparent high incidence of melanoma most likely reflects referral/publication bias rather than a statistically significant association. In fact, the clinical lesion most clinically similar to hairy NS is Becker nevus, with tan macules demonstrating lentiginous melanocytic hyperplasia associated with numerous coarse terminal hairs. There is no indication that Becker nevi have a considerable premalignant potential, though one case of melanoma arising in a Becker nevus has been reported.9 There is no evidence to suggest that classic CMN with hypertrichosis has a greater premalignant potential than similar lesions without hypertrichosis.


We noticed the presence of hair in our patient’s lesion only after reports in the literature caused us to look for this phenomenon.9 This occurrence may actually be quite common. We do not recommend prophylactic excision of NS and believe the risk for malignant degeneration is low in NS with or without hair, though larger NS (>4 cm), especially giant, zosteriform, or segmental lesions, may have a greater risk.1,6,9,10 It is prudent for physicians to carefully examine NS and sample suspicious foci, especially when patients describe a lesion as changing.

References
  1. Vidaurri-de la Cruz H, Happle R. Two distinct types of speckled lentiginous nevi characterized by macular versus papular speckles. Dermatology. 2006;212:53-58.
  2. Ly L, Christie M, Swain S, et al. Melanoma(s) arising in large segmental speckled lentiginous nevi: a case series. J Am Acad Dermatol. 2011;64:1190-1193.
  3. Prose NS, Heilman E, Felman YM, et al. Multiple benign juvenile melanoma. J Am Acad Dermatol. 1983;9:236-242.
  4. Grinspan D, Casala A, Abulafia J, et al. Melanoma on dysplastic nevus spilus. Int J Dermatol. 1997;36:499-502 .
  5. Langenbach N, Pfau A, Landthaler M, et al. Naevi spili, café-au-lait spots and melanocytic naevi aggregated alongside Blaschko’s lines, with a review of segmental melanocytic lesions. Acta Derm Venereol. 1998;78:378-380.
  6. Schaffer JV, Orlow SJ, Lazova R, et al. Speckled lentiginous nevus: within the spectrum of congenital melanocytic nevi. Arch Dermatol. 2001;137:172-178.
  7. Saraswat A, Dogra S, Bansali A, et al. Phakomatosis pigmentokeratotica associated with hypophosphataemic vitamin D–resistant rickets: improvement in phosphate homeostasis after partial laser ablation. Br J Dermatol. 2003;148:1074-1076.
  8. Zeren-Bilgin i, Gür S, Aydın O, et al. Melanoma arising in a hairy nevus spilus. Int J Dermatol. 2006;45:1362-1364.
  9. Singh S, Jain N, Khanna N, et al. Hairy nevus spilus: a case series. Pediatr Dermatol. 2013;30:100-104.
  10. Price HN, Schaffer JV. Congenital melanocytic nevi—when to worry and how to treat: facts and controversies. Clin Dermatol. 2010;28:293-302.
  11. Alikhan Ali, Ibrahimi OA, Eisen DB. Congenital melanocytic nevi: where are we now? J Am Acad Dermatol. 2012;67:495.e1-495.e17.
  12. Haenssle HA, Kaune KM, Buhl T, et al. Melanoma arising in segmental nevus spilus: detection by sequential digital dermatoscopy. J Am Acad Dermatol. 2009;61:337-341.
  13. Cohen LM. Nevus spilus: congenital or acquired? Arch Dermatol. 2001;137:215-216.
References
  1. Vidaurri-de la Cruz H, Happle R. Two distinct types of speckled lentiginous nevi characterized by macular versus papular speckles. Dermatology. 2006;212:53-58.
  2. Ly L, Christie M, Swain S, et al. Melanoma(s) arising in large segmental speckled lentiginous nevi: a case series. J Am Acad Dermatol. 2011;64:1190-1193.
  3. Prose NS, Heilman E, Felman YM, et al. Multiple benign juvenile melanoma. J Am Acad Dermatol. 1983;9:236-242.
  4. Grinspan D, Casala A, Abulafia J, et al. Melanoma on dysplastic nevus spilus. Int J Dermatol. 1997;36:499-502 .
  5. Langenbach N, Pfau A, Landthaler M, et al. Naevi spili, café-au-lait spots and melanocytic naevi aggregated alongside Blaschko’s lines, with a review of segmental melanocytic lesions. Acta Derm Venereol. 1998;78:378-380.
  6. Schaffer JV, Orlow SJ, Lazova R, et al. Speckled lentiginous nevus: within the spectrum of congenital melanocytic nevi. Arch Dermatol. 2001;137:172-178.
  7. Saraswat A, Dogra S, Bansali A, et al. Phakomatosis pigmentokeratotica associated with hypophosphataemic vitamin D–resistant rickets: improvement in phosphate homeostasis after partial laser ablation. Br J Dermatol. 2003;148:1074-1076.
  8. Zeren-Bilgin i, Gür S, Aydın O, et al. Melanoma arising in a hairy nevus spilus. Int J Dermatol. 2006;45:1362-1364.
  9. Singh S, Jain N, Khanna N, et al. Hairy nevus spilus: a case series. Pediatr Dermatol. 2013;30:100-104.
  10. Price HN, Schaffer JV. Congenital melanocytic nevi—when to worry and how to treat: facts and controversies. Clin Dermatol. 2010;28:293-302.
  11. Alikhan Ali, Ibrahimi OA, Eisen DB. Congenital melanocytic nevi: where are we now? J Am Acad Dermatol. 2012;67:495.e1-495.e17.
  12. Haenssle HA, Kaune KM, Buhl T, et al. Melanoma arising in segmental nevus spilus: detection by sequential digital dermatoscopy. J Am Acad Dermatol. 2009;61:337-341.
  13. Cohen LM. Nevus spilus: congenital or acquired? Arch Dermatol. 2001;137:215-216.
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Nevus Spilus: Is the Presence of Hair Associated With an Increased Risk for Melanoma?
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Practice Points

  • Nevus spilus (NS) appears as a café au lait macule studded with darker brown “moles.”
  • Although melanoma has been described in NS, it is rare.
  • There is no evidence that hairy NS are predisposed to melanoma.
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Melanoma Registry Underreporting in the Veterans Health Administration

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Melanoma Registry Underreporting in the Veterans Health Administration
Use of local SNOMED codes and clerical errors led to the underreporting of melanomas despite having an in-house reporting system and understanding reporting requirements.

The National Cancer Data Base (NCDB) of the American College of Surgeons (ACS), the Surveillance, Epidemiology, and End Results (SEER) program of the National Cancer Institute (NCI), and the National Program of Cancer Registries (NPCR) of the Centers for Disease Control and Prevention (CDC) are among the leading registries for cancer surveillance, collecting cancer epidemiology data for the majority of the U.S. population.1 This national coverage aids researchers and policymakers in conducting epidemiologic studies and allocating health resources.1,2

U.S. federal law mandates the reporting of cancer.3,4 State laws require cancer reporting as well, but requirements vary slightly from state to state.5 However, all cancers with an ICD-O (International Classification of Diseases for Oncology) code of 2 or 3 are reportable. For Washington state, cancer must be reported unless it is basal or squamous cell carcinoma of nonmucoepidermoid skin or in situ cancer of the uterine cervix.5 In general, each facility that diagnoses or treats a melanoma is required to report it. Data are consolidated at the central registry level if necessary.

Cancer reporting often fails to meet states’ requirements.6-8 Since the inception of SEER and NPCR, many studies have assessed the accuracy of the cancer data reported to these registries and have found these data to be inaccurate or incomplete.6-8 Melanoma reporting, in particular,
seems to be prone to error. Studies have demonstrated melanoma underreporting ranging from 10% to 70%, with an increase in underreporting over time.9-11 Significant delays of up to 10 years have been found between initial diagnosis and reporting for melanomas.12 In general, these studies have focused on smaller facilities, such as private laboratories, which lack in-house reporting systems.

Cancer reporting is especially important in the VHA, the largest U.S. health care system. Health data on about 9 million enrolled veterans have been invaluable for understanding cancer epidemiology. Underreporting and misreporting of cancer cases in private medical offices and smaller treatment facilities may be attributable to lack of funding, personnel, administrative support, or knowledge of reporting requirements. In contrast, the VHA requires cancer reporting and provides funding, personnel, and administrative support.13

The VA Puget Sound Health Care System (VAPSHCS) traditionally has employed registrars to perform the majority of basic cancer registry tasks, including abstracting, case finding, and lifelong follow-up of the cancer patients listed in the registry. The registrars use OncoTraX software, which finds possible cancer cases from pathology, radiology, and patient treatment files, to accession cases. Unique cancer cases are reported to the VA Central Cancer Registry (VACCR), the Washington state registry, and the NCDB, which then transfer the data to the national registries. Accordingly, cases not accessioned would not be reported to the VA, state, and national registries.

The authors conducted a quality improvement project to ascertain whether primary cutaneous melanomas biopsied at VAPSHCS were underreported.

Materials

The VAPSHCS serves about 100,000 veterans and consists of 2 major treatment facilities, 2 community-based outpatient clinics, 1 outreach clinic, and 4 contract community-based outpatient clinics. Pathology cases for the entire VAPSHCS are accessioned in a central laboratory in Seattle.

Data Sources and Chart Abstraction

Data sources included the VA Corporate Data Warehouse (CDW), the VAPSHCS cancer registry, the Computerized Patient Record System (CPRS), VistA (Veterans Health Information Systems and Technology Architecture), VistA Web, and VistA Imaging.

Study Population

The study population consisted of veterans who had been diagnosed with primary cutaneous melanoma and had the diagnosis confirmed by biopsy performed at VAPSHCS between January 1, 2006 and December 31, 2012.

Statistical Analysis

Odds ratios were calculated using the MedCalc Odds Ratio Calculator.14

 

 

Methods

The authors identified SNOMED (Systematized Nomenclature of Medicine) codes that included the character string melanoma (Table 1). Using these codes, they queried VistA to identify melanoma cases diagnosed in the VAPSHCS Pathology and Laboratory Service during the period 2006 to 2012. To confirm the completeness of the local report, the authors performed the same search using the CDW. The SNOMED code case-finding was supplemented with cases ascertained using ICD-9 codes and problem list diagnoses.

A case must be reported to the local cancer registry if diagnosis or treatment takes place at the facility. All cases ascertained with the authors’ search criteria are, by definition, reportable to the local cancer registry. The authors then applied inclusion and exclusion criteria to determine
which cases were primary cutaneous melanomas and therefore candidates for this investigation (Table 2).

Having ascertained the primary cutaneous melanomas, the authors abstracted the pathology TNM (tumor, node, metastasis) staging (Breslow depth, mitotic index, presence of ulceration) and diagnosis dates from CPRS pathology reports. They then determined whether each case had been reported to the VACCR (OncoTraX was used to query for the accession status of each melanoma). If the melanoma was not accessioned, the authors tried to determine why.

 

Results

The authors discovered 193 primary cutaneous melanomas diagnosed by biopsy performed at VAPSHCS. Of these 193 melanomas, 71 (36.8%) had not been reported.

After the pathologist has completed a report, SNOMED codes are assigned by the pathology laboratory. Case finding with OncoTraX depends on SNOMED codes and other parameters (imaging, treatment, oncology consultation). OncoTraX is designed for case finding using World Health Organization (WHO) standardized 8000/X-9000/X series SNOMED codes. To understand the relationship between reporting and SNOMED codes, the authors ascertained the codes for all melanomas in the present study.

Table 3 lists the SNOMED codes assigned to melanomas biopsied at VAPSHCS and the percentage reported for each. Of the 106 melanomas that had been assigned WHO standardized codes, 101 (95.2%) had been reported. In contrast, only 21 (24.1%) of the 87 melanomas that had been assigned non-WHO standardized codes had been reported. In this study, non-WHO standardized codes are locally generated codes; they began with facility station number 663.

Use of locally generated codes may have contributed to nonreporting. Of the 71 melanomas not reported, 66 had a SNOMED code beginning with 663, and the other 5 had a WHO standardized SNOMED code. Odds of being nonreported were much higher for the melanomas with 663 codes than for the melanomas with WHO standardized codes (odds ratio [OR], 63.5; confidence interval [CI], 22.8-176.7; P ≤ .0001).

There was also a difference in coding between invasive and in situ melanomas. Of the 87 melanomas with a 663 code, 68 were in situ. Of the 106 melanomas with a national-level code, 11 were in situ. The odds of being assigned a local code were much higher for the in situ melanomas than they were for the invasive melanomas (OR, 30.9; CI, 13.8-69.1; P ≤ .0001).

Since 2000, the SNOMED code for melanoma in situ has been 87202, but no melanomas in situ were assigned this code. The 87202 code was not available in VistA for pathology laboratories to assign to melanomas at the time this study was conducted. Instead, most melanomas in situ were assigned a locally generated code. However, OncoTraX cannot recognize local codes, so melanomas assigned a local code might not have been accessionable.

The remaining 5 unreported melanomas were assigned WHO standardized codes. Secondary analysis revealed clerical errors, 4 made by the pathology laboratory and 1 by the registrar.

 

 

Discussion

Data from central cancer registries are used in a variety of fields, from research studies to health policymaking. They are used to “monitor cancer trends over time, show cancer patterns in various populations, identify high-risk groups, guide planning and evaluation of cancer control programs, help set priorities for allocating health resources, and advance clinical, epidemiologic, and health services research.”1

Melanoma underreporting has been demonstrated in previous studies, with the percentage of underreported cases varying from 10.4%11 to 70%.9 A longitudinal study of melanomas in Washington state found that underreporting of cutaneous melanomas increased from 2% to 21% over a 10-year period.10 This trend prompted examination of this study’s data for a similar temporal trend, and none was found.

A 2008 study found that more melanoma cases were being diagnosed or treated at outpatient facilities.9 Such facilities are prone to problems in reporting because they lack in-house reporting systems and knowledge of melanoma reporting requirements.9 A 2011 study of
practicing dermatologists found that many failed to report melanomas to a registry, and more than half were unaware of the requirement.12 Accordingly, underreporting is likely to continue. Results of the present study showed that melanoma underreporting was a major issue at VAPSHCS and that it could occur even in facilities that used in-house reporting systems and were aware of reporting requirements. The primary cause of underreporting was generation and use of local SNOMED codes that were unrecognizable by OncoTraX. A secondary cause was clerical error.

Discovery of unreported cases prompted facility review of procedures for reporting melanomas and expansion of current methods for melanoma discovery. All unreported cases have been entered into the VACCR, the Washington state registry, and the NCDB, which populate the national cancer registries. Contract registry staff were educated regarding melanoma reporting requirements, particularly requirements for melanoma in situ. The 87202 SNOMED code for melanoma in situ also has been added to VistA at VAPSHCS. A follow-up study will be conducted to ascertain whether the interventions have corrected the underreporting of melanoma.

Study Limitations

The cases used in the study were obtained by SNOMED codes, CDW problem lists, and ICD-9 codes. This method may have missed cases that were assigned incorrect SNOMED codes and were not assigned to the problem list, or that were assigned to the problem list after the study period. The authors used a subset of all reportable cases—namely, those biopsied at VAPSHCS. Although this subset constituted the significant majority of reportable cases, the authors do not know the extent of underreporting of cases that were not biopsied at VAPSHCS. The extent to which other VA facilities generate local SNOMED codes also is unknown.

Conclusion

Melanoma underreporting at VAPSHCS is an addressable concern. The primary cause of underreporting was the use of locally generated SNOMED codes that were not recognized by cancer registry software. The present study should be repeated at other VA facilities to determine the extent to which its findings are generalizable.

Acknowledgments
The authors thank Dr. Stevan Knezevich for reviewing cases, Pam Pehan for providing the list of VAPSHCS melanomas accessioned from VistA, and Eddie Alaniz and Eugene Gavrilenko for helping ascertain SNOMED codes.

Author disclosures
The authors report no actual or potential conflicts of interest with regard to this article.

Disclaimer
The opinions expressed herein are those of the authors and do not necessarily reflect those of Federal Practitioner, Frontline Medical Communications Inc., the U.S. Government, or any of its agencies. This article may discuss unlabeled or investigational use of certain drugs. Please review the complete prescribing information for specific drugs or drug combinations—including indications, contraindications, warnings, and adverse effects—before administering pharmacologic therapy to patients.

 

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References

1. Division of Cancer Prevention and Control, Centers for Disease Control and Prevention. National Program of Cancer Registries (NPCR). CDC website. http://www.cdc.gov/cancer/npcr/about.htm. Updated April 20, 2016. Accessed July 1, 2016.

2. National Cancer Institute. Overview of the SEER program. National Cancer Institute website. http://seer.cancer.gov/about/overview.html. Accessed July 18, 2016.

3. Cancer Registries Amendment Act. 42 USC §201-280e (2016).

4. Cancer Registry of Greater California. Cancer reporting. Cancer Registry of Greater California website. http://crgc-cancer.org/hospitals-and-physicians. Accessed July 18, 2016.

5. American Academy of Dermatology. State cancer registry laws and requirements. American Academy of Dermatology website. https://www.aad.org/file%20library/global%20navigatio/education%20and%20quality%20care/state%20cancer%20registries/state-cancer-registries-laws-and-requirements.pdf. Accessed July 18, 2016.

6. Craig BM, Rollison DE, List AF, Cogle CR. Underreporting of myeloid malignancies by United States cancer registries. Cancer Epidemiol Biomarkers Prev. 2012;21(3):474-481.

7. Fanning J, Gangestad A, Andrews SJ. National Cancer Data Base/Surveillance Epidemiology and End Results: potential insensitive-measure bias. Gynecol Oncol. 2000;77(3):450-453.

8. Thoburn KK, German RR, Lewis M, Nichols PJ, Ahmed F, Jackson-Thompson J. Case completeness and data accuracy in the Centers for Disease Control and Prevention’s National Program of Cancer Registries. Cancer. 2007;109(8):1607-1616.

9. Cockburn M, Swetter SM, Peng D, Keegan TH, Deapen D, Clarke CA. Melanoma underreporting: why does it happen, how big is the problem, and how do we fix it? J Am Acad Dermatol. 2008;59(6):1081-1085.

10. Karagas MR, Thomas DB, Roth GJ, Johnson LK, Weiss NS. The effects of changes in health care delivery on the reported incidence of cutaneous melanoma in western Washington state. Am J Epidemiol. 1991;133(1):58-62.

11. Merlino LA, Sullivan KJ, Whitaker DC, Lynch CF. The independent pathology laboratory as a reporting source for cutaneous melanoma incidence in Iowa, 1977–1994. J Am Acad Dermatol. 1997;37(4):578-585.

12. Cartee TV, Kini SP, Chen SC. Melanoma reporting to central cancer registries by US dermatologists: an analysis of the persistent knowledge and practice gap. J Am Acad Dermatol. 2011;65(5)(suppl 1):S124-S132.

13. Clegg LX, Feuer EJ, Midthune DN, Fay MP, Hankey BF. Impact of reporting delay and reporting error on cancer incidence rates and trends. J Natl Cancer Inst. 2002;94(20):1537-1545.

14. Odds ratio calculator. MedCalc website. https://www.medcalc.org/calc/odds_ratio.php. Accessed June 16, 2016.

Note: Page numbers differ between the print issue and digital edition.

Author and Disclosure Information

Dr. Raugi is a physician, and Ms. Das is the cancer care program manager, both at VA Puget Sound Health Care System. Mr. Markham is the VISN 20 data manager for the Store and Forward Teledermatology Program. Dr. Raugi is a professor of dermatology, and Ms. Dougall, Mr. Gendreau, Ms. Capulong, Mr. Lau, and Mr. Gemelas are students; all at the University of Washington in Seattle.

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Dr. Raugi is a physician, and Ms. Das is the cancer care program manager, both at VA Puget Sound Health Care System. Mr. Markham is the VISN 20 data manager for the Store and Forward Teledermatology Program. Dr. Raugi is a professor of dermatology, and Ms. Dougall, Mr. Gendreau, Ms. Capulong, Mr. Lau, and Mr. Gemelas are students; all at the University of Washington in Seattle.

Author and Disclosure Information

Dr. Raugi is a physician, and Ms. Das is the cancer care program manager, both at VA Puget Sound Health Care System. Mr. Markham is the VISN 20 data manager for the Store and Forward Teledermatology Program. Dr. Raugi is a professor of dermatology, and Ms. Dougall, Mr. Gendreau, Ms. Capulong, Mr. Lau, and Mr. Gemelas are students; all at the University of Washington in Seattle.

Use of local SNOMED codes and clerical errors led to the underreporting of melanomas despite having an in-house reporting system and understanding reporting requirements.
Use of local SNOMED codes and clerical errors led to the underreporting of melanomas despite having an in-house reporting system and understanding reporting requirements.

The National Cancer Data Base (NCDB) of the American College of Surgeons (ACS), the Surveillance, Epidemiology, and End Results (SEER) program of the National Cancer Institute (NCI), and the National Program of Cancer Registries (NPCR) of the Centers for Disease Control and Prevention (CDC) are among the leading registries for cancer surveillance, collecting cancer epidemiology data for the majority of the U.S. population.1 This national coverage aids researchers and policymakers in conducting epidemiologic studies and allocating health resources.1,2

U.S. federal law mandates the reporting of cancer.3,4 State laws require cancer reporting as well, but requirements vary slightly from state to state.5 However, all cancers with an ICD-O (International Classification of Diseases for Oncology) code of 2 or 3 are reportable. For Washington state, cancer must be reported unless it is basal or squamous cell carcinoma of nonmucoepidermoid skin or in situ cancer of the uterine cervix.5 In general, each facility that diagnoses or treats a melanoma is required to report it. Data are consolidated at the central registry level if necessary.

Cancer reporting often fails to meet states’ requirements.6-8 Since the inception of SEER and NPCR, many studies have assessed the accuracy of the cancer data reported to these registries and have found these data to be inaccurate or incomplete.6-8 Melanoma reporting, in particular,
seems to be prone to error. Studies have demonstrated melanoma underreporting ranging from 10% to 70%, with an increase in underreporting over time.9-11 Significant delays of up to 10 years have been found between initial diagnosis and reporting for melanomas.12 In general, these studies have focused on smaller facilities, such as private laboratories, which lack in-house reporting systems.

Cancer reporting is especially important in the VHA, the largest U.S. health care system. Health data on about 9 million enrolled veterans have been invaluable for understanding cancer epidemiology. Underreporting and misreporting of cancer cases in private medical offices and smaller treatment facilities may be attributable to lack of funding, personnel, administrative support, or knowledge of reporting requirements. In contrast, the VHA requires cancer reporting and provides funding, personnel, and administrative support.13

The VA Puget Sound Health Care System (VAPSHCS) traditionally has employed registrars to perform the majority of basic cancer registry tasks, including abstracting, case finding, and lifelong follow-up of the cancer patients listed in the registry. The registrars use OncoTraX software, which finds possible cancer cases from pathology, radiology, and patient treatment files, to accession cases. Unique cancer cases are reported to the VA Central Cancer Registry (VACCR), the Washington state registry, and the NCDB, which then transfer the data to the national registries. Accordingly, cases not accessioned would not be reported to the VA, state, and national registries.

The authors conducted a quality improvement project to ascertain whether primary cutaneous melanomas biopsied at VAPSHCS were underreported.

Materials

The VAPSHCS serves about 100,000 veterans and consists of 2 major treatment facilities, 2 community-based outpatient clinics, 1 outreach clinic, and 4 contract community-based outpatient clinics. Pathology cases for the entire VAPSHCS are accessioned in a central laboratory in Seattle.

Data Sources and Chart Abstraction

Data sources included the VA Corporate Data Warehouse (CDW), the VAPSHCS cancer registry, the Computerized Patient Record System (CPRS), VistA (Veterans Health Information Systems and Technology Architecture), VistA Web, and VistA Imaging.

Study Population

The study population consisted of veterans who had been diagnosed with primary cutaneous melanoma and had the diagnosis confirmed by biopsy performed at VAPSHCS between January 1, 2006 and December 31, 2012.

Statistical Analysis

Odds ratios were calculated using the MedCalc Odds Ratio Calculator.14

 

 

Methods

The authors identified SNOMED (Systematized Nomenclature of Medicine) codes that included the character string melanoma (Table 1). Using these codes, they queried VistA to identify melanoma cases diagnosed in the VAPSHCS Pathology and Laboratory Service during the period 2006 to 2012. To confirm the completeness of the local report, the authors performed the same search using the CDW. The SNOMED code case-finding was supplemented with cases ascertained using ICD-9 codes and problem list diagnoses.

A case must be reported to the local cancer registry if diagnosis or treatment takes place at the facility. All cases ascertained with the authors’ search criteria are, by definition, reportable to the local cancer registry. The authors then applied inclusion and exclusion criteria to determine
which cases were primary cutaneous melanomas and therefore candidates for this investigation (Table 2).

Having ascertained the primary cutaneous melanomas, the authors abstracted the pathology TNM (tumor, node, metastasis) staging (Breslow depth, mitotic index, presence of ulceration) and diagnosis dates from CPRS pathology reports. They then determined whether each case had been reported to the VACCR (OncoTraX was used to query for the accession status of each melanoma). If the melanoma was not accessioned, the authors tried to determine why.

 

Results

The authors discovered 193 primary cutaneous melanomas diagnosed by biopsy performed at VAPSHCS. Of these 193 melanomas, 71 (36.8%) had not been reported.

After the pathologist has completed a report, SNOMED codes are assigned by the pathology laboratory. Case finding with OncoTraX depends on SNOMED codes and other parameters (imaging, treatment, oncology consultation). OncoTraX is designed for case finding using World Health Organization (WHO) standardized 8000/X-9000/X series SNOMED codes. To understand the relationship between reporting and SNOMED codes, the authors ascertained the codes for all melanomas in the present study.

Table 3 lists the SNOMED codes assigned to melanomas biopsied at VAPSHCS and the percentage reported for each. Of the 106 melanomas that had been assigned WHO standardized codes, 101 (95.2%) had been reported. In contrast, only 21 (24.1%) of the 87 melanomas that had been assigned non-WHO standardized codes had been reported. In this study, non-WHO standardized codes are locally generated codes; they began with facility station number 663.

Use of locally generated codes may have contributed to nonreporting. Of the 71 melanomas not reported, 66 had a SNOMED code beginning with 663, and the other 5 had a WHO standardized SNOMED code. Odds of being nonreported were much higher for the melanomas with 663 codes than for the melanomas with WHO standardized codes (odds ratio [OR], 63.5; confidence interval [CI], 22.8-176.7; P ≤ .0001).

There was also a difference in coding between invasive and in situ melanomas. Of the 87 melanomas with a 663 code, 68 were in situ. Of the 106 melanomas with a national-level code, 11 were in situ. The odds of being assigned a local code were much higher for the in situ melanomas than they were for the invasive melanomas (OR, 30.9; CI, 13.8-69.1; P ≤ .0001).

Since 2000, the SNOMED code for melanoma in situ has been 87202, but no melanomas in situ were assigned this code. The 87202 code was not available in VistA for pathology laboratories to assign to melanomas at the time this study was conducted. Instead, most melanomas in situ were assigned a locally generated code. However, OncoTraX cannot recognize local codes, so melanomas assigned a local code might not have been accessionable.

The remaining 5 unreported melanomas were assigned WHO standardized codes. Secondary analysis revealed clerical errors, 4 made by the pathology laboratory and 1 by the registrar.

 

 

Discussion

Data from central cancer registries are used in a variety of fields, from research studies to health policymaking. They are used to “monitor cancer trends over time, show cancer patterns in various populations, identify high-risk groups, guide planning and evaluation of cancer control programs, help set priorities for allocating health resources, and advance clinical, epidemiologic, and health services research.”1

Melanoma underreporting has been demonstrated in previous studies, with the percentage of underreported cases varying from 10.4%11 to 70%.9 A longitudinal study of melanomas in Washington state found that underreporting of cutaneous melanomas increased from 2% to 21% over a 10-year period.10 This trend prompted examination of this study’s data for a similar temporal trend, and none was found.

A 2008 study found that more melanoma cases were being diagnosed or treated at outpatient facilities.9 Such facilities are prone to problems in reporting because they lack in-house reporting systems and knowledge of melanoma reporting requirements.9 A 2011 study of
practicing dermatologists found that many failed to report melanomas to a registry, and more than half were unaware of the requirement.12 Accordingly, underreporting is likely to continue. Results of the present study showed that melanoma underreporting was a major issue at VAPSHCS and that it could occur even in facilities that used in-house reporting systems and were aware of reporting requirements. The primary cause of underreporting was generation and use of local SNOMED codes that were unrecognizable by OncoTraX. A secondary cause was clerical error.

Discovery of unreported cases prompted facility review of procedures for reporting melanomas and expansion of current methods for melanoma discovery. All unreported cases have been entered into the VACCR, the Washington state registry, and the NCDB, which populate the national cancer registries. Contract registry staff were educated regarding melanoma reporting requirements, particularly requirements for melanoma in situ. The 87202 SNOMED code for melanoma in situ also has been added to VistA at VAPSHCS. A follow-up study will be conducted to ascertain whether the interventions have corrected the underreporting of melanoma.

Study Limitations

The cases used in the study were obtained by SNOMED codes, CDW problem lists, and ICD-9 codes. This method may have missed cases that were assigned incorrect SNOMED codes and were not assigned to the problem list, or that were assigned to the problem list after the study period. The authors used a subset of all reportable cases—namely, those biopsied at VAPSHCS. Although this subset constituted the significant majority of reportable cases, the authors do not know the extent of underreporting of cases that were not biopsied at VAPSHCS. The extent to which other VA facilities generate local SNOMED codes also is unknown.

Conclusion

Melanoma underreporting at VAPSHCS is an addressable concern. The primary cause of underreporting was the use of locally generated SNOMED codes that were not recognized by cancer registry software. The present study should be repeated at other VA facilities to determine the extent to which its findings are generalizable.

Acknowledgments
The authors thank Dr. Stevan Knezevich for reviewing cases, Pam Pehan for providing the list of VAPSHCS melanomas accessioned from VistA, and Eddie Alaniz and Eugene Gavrilenko for helping ascertain SNOMED codes.

Author disclosures
The authors report no actual or potential conflicts of interest with regard to this article.

Disclaimer
The opinions expressed herein are those of the authors and do not necessarily reflect those of Federal Practitioner, Frontline Medical Communications Inc., the U.S. Government, or any of its agencies. This article may discuss unlabeled or investigational use of certain drugs. Please review the complete prescribing information for specific drugs or drug combinations—including indications, contraindications, warnings, and adverse effects—before administering pharmacologic therapy to patients.

 

Click here to read the digital edition.

The National Cancer Data Base (NCDB) of the American College of Surgeons (ACS), the Surveillance, Epidemiology, and End Results (SEER) program of the National Cancer Institute (NCI), and the National Program of Cancer Registries (NPCR) of the Centers for Disease Control and Prevention (CDC) are among the leading registries for cancer surveillance, collecting cancer epidemiology data for the majority of the U.S. population.1 This national coverage aids researchers and policymakers in conducting epidemiologic studies and allocating health resources.1,2

U.S. federal law mandates the reporting of cancer.3,4 State laws require cancer reporting as well, but requirements vary slightly from state to state.5 However, all cancers with an ICD-O (International Classification of Diseases for Oncology) code of 2 or 3 are reportable. For Washington state, cancer must be reported unless it is basal or squamous cell carcinoma of nonmucoepidermoid skin or in situ cancer of the uterine cervix.5 In general, each facility that diagnoses or treats a melanoma is required to report it. Data are consolidated at the central registry level if necessary.

Cancer reporting often fails to meet states’ requirements.6-8 Since the inception of SEER and NPCR, many studies have assessed the accuracy of the cancer data reported to these registries and have found these data to be inaccurate or incomplete.6-8 Melanoma reporting, in particular,
seems to be prone to error. Studies have demonstrated melanoma underreporting ranging from 10% to 70%, with an increase in underreporting over time.9-11 Significant delays of up to 10 years have been found between initial diagnosis and reporting for melanomas.12 In general, these studies have focused on smaller facilities, such as private laboratories, which lack in-house reporting systems.

Cancer reporting is especially important in the VHA, the largest U.S. health care system. Health data on about 9 million enrolled veterans have been invaluable for understanding cancer epidemiology. Underreporting and misreporting of cancer cases in private medical offices and smaller treatment facilities may be attributable to lack of funding, personnel, administrative support, or knowledge of reporting requirements. In contrast, the VHA requires cancer reporting and provides funding, personnel, and administrative support.13

The VA Puget Sound Health Care System (VAPSHCS) traditionally has employed registrars to perform the majority of basic cancer registry tasks, including abstracting, case finding, and lifelong follow-up of the cancer patients listed in the registry. The registrars use OncoTraX software, which finds possible cancer cases from pathology, radiology, and patient treatment files, to accession cases. Unique cancer cases are reported to the VA Central Cancer Registry (VACCR), the Washington state registry, and the NCDB, which then transfer the data to the national registries. Accordingly, cases not accessioned would not be reported to the VA, state, and national registries.

The authors conducted a quality improvement project to ascertain whether primary cutaneous melanomas biopsied at VAPSHCS were underreported.

Materials

The VAPSHCS serves about 100,000 veterans and consists of 2 major treatment facilities, 2 community-based outpatient clinics, 1 outreach clinic, and 4 contract community-based outpatient clinics. Pathology cases for the entire VAPSHCS are accessioned in a central laboratory in Seattle.

Data Sources and Chart Abstraction

Data sources included the VA Corporate Data Warehouse (CDW), the VAPSHCS cancer registry, the Computerized Patient Record System (CPRS), VistA (Veterans Health Information Systems and Technology Architecture), VistA Web, and VistA Imaging.

Study Population

The study population consisted of veterans who had been diagnosed with primary cutaneous melanoma and had the diagnosis confirmed by biopsy performed at VAPSHCS between January 1, 2006 and December 31, 2012.

Statistical Analysis

Odds ratios were calculated using the MedCalc Odds Ratio Calculator.14

 

 

Methods

The authors identified SNOMED (Systematized Nomenclature of Medicine) codes that included the character string melanoma (Table 1). Using these codes, they queried VistA to identify melanoma cases diagnosed in the VAPSHCS Pathology and Laboratory Service during the period 2006 to 2012. To confirm the completeness of the local report, the authors performed the same search using the CDW. The SNOMED code case-finding was supplemented with cases ascertained using ICD-9 codes and problem list diagnoses.

A case must be reported to the local cancer registry if diagnosis or treatment takes place at the facility. All cases ascertained with the authors’ search criteria are, by definition, reportable to the local cancer registry. The authors then applied inclusion and exclusion criteria to determine
which cases were primary cutaneous melanomas and therefore candidates for this investigation (Table 2).

Having ascertained the primary cutaneous melanomas, the authors abstracted the pathology TNM (tumor, node, metastasis) staging (Breslow depth, mitotic index, presence of ulceration) and diagnosis dates from CPRS pathology reports. They then determined whether each case had been reported to the VACCR (OncoTraX was used to query for the accession status of each melanoma). If the melanoma was not accessioned, the authors tried to determine why.

 

Results

The authors discovered 193 primary cutaneous melanomas diagnosed by biopsy performed at VAPSHCS. Of these 193 melanomas, 71 (36.8%) had not been reported.

After the pathologist has completed a report, SNOMED codes are assigned by the pathology laboratory. Case finding with OncoTraX depends on SNOMED codes and other parameters (imaging, treatment, oncology consultation). OncoTraX is designed for case finding using World Health Organization (WHO) standardized 8000/X-9000/X series SNOMED codes. To understand the relationship between reporting and SNOMED codes, the authors ascertained the codes for all melanomas in the present study.

Table 3 lists the SNOMED codes assigned to melanomas biopsied at VAPSHCS and the percentage reported for each. Of the 106 melanomas that had been assigned WHO standardized codes, 101 (95.2%) had been reported. In contrast, only 21 (24.1%) of the 87 melanomas that had been assigned non-WHO standardized codes had been reported. In this study, non-WHO standardized codes are locally generated codes; they began with facility station number 663.

Use of locally generated codes may have contributed to nonreporting. Of the 71 melanomas not reported, 66 had a SNOMED code beginning with 663, and the other 5 had a WHO standardized SNOMED code. Odds of being nonreported were much higher for the melanomas with 663 codes than for the melanomas with WHO standardized codes (odds ratio [OR], 63.5; confidence interval [CI], 22.8-176.7; P ≤ .0001).

There was also a difference in coding between invasive and in situ melanomas. Of the 87 melanomas with a 663 code, 68 were in situ. Of the 106 melanomas with a national-level code, 11 were in situ. The odds of being assigned a local code were much higher for the in situ melanomas than they were for the invasive melanomas (OR, 30.9; CI, 13.8-69.1; P ≤ .0001).

Since 2000, the SNOMED code for melanoma in situ has been 87202, but no melanomas in situ were assigned this code. The 87202 code was not available in VistA for pathology laboratories to assign to melanomas at the time this study was conducted. Instead, most melanomas in situ were assigned a locally generated code. However, OncoTraX cannot recognize local codes, so melanomas assigned a local code might not have been accessionable.

The remaining 5 unreported melanomas were assigned WHO standardized codes. Secondary analysis revealed clerical errors, 4 made by the pathology laboratory and 1 by the registrar.

 

 

Discussion

Data from central cancer registries are used in a variety of fields, from research studies to health policymaking. They are used to “monitor cancer trends over time, show cancer patterns in various populations, identify high-risk groups, guide planning and evaluation of cancer control programs, help set priorities for allocating health resources, and advance clinical, epidemiologic, and health services research.”1

Melanoma underreporting has been demonstrated in previous studies, with the percentage of underreported cases varying from 10.4%11 to 70%.9 A longitudinal study of melanomas in Washington state found that underreporting of cutaneous melanomas increased from 2% to 21% over a 10-year period.10 This trend prompted examination of this study’s data for a similar temporal trend, and none was found.

A 2008 study found that more melanoma cases were being diagnosed or treated at outpatient facilities.9 Such facilities are prone to problems in reporting because they lack in-house reporting systems and knowledge of melanoma reporting requirements.9 A 2011 study of
practicing dermatologists found that many failed to report melanomas to a registry, and more than half were unaware of the requirement.12 Accordingly, underreporting is likely to continue. Results of the present study showed that melanoma underreporting was a major issue at VAPSHCS and that it could occur even in facilities that used in-house reporting systems and were aware of reporting requirements. The primary cause of underreporting was generation and use of local SNOMED codes that were unrecognizable by OncoTraX. A secondary cause was clerical error.

Discovery of unreported cases prompted facility review of procedures for reporting melanomas and expansion of current methods for melanoma discovery. All unreported cases have been entered into the VACCR, the Washington state registry, and the NCDB, which populate the national cancer registries. Contract registry staff were educated regarding melanoma reporting requirements, particularly requirements for melanoma in situ. The 87202 SNOMED code for melanoma in situ also has been added to VistA at VAPSHCS. A follow-up study will be conducted to ascertain whether the interventions have corrected the underreporting of melanoma.

Study Limitations

The cases used in the study were obtained by SNOMED codes, CDW problem lists, and ICD-9 codes. This method may have missed cases that were assigned incorrect SNOMED codes and were not assigned to the problem list, or that were assigned to the problem list after the study period. The authors used a subset of all reportable cases—namely, those biopsied at VAPSHCS. Although this subset constituted the significant majority of reportable cases, the authors do not know the extent of underreporting of cases that were not biopsied at VAPSHCS. The extent to which other VA facilities generate local SNOMED codes also is unknown.

Conclusion

Melanoma underreporting at VAPSHCS is an addressable concern. The primary cause of underreporting was the use of locally generated SNOMED codes that were not recognized by cancer registry software. The present study should be repeated at other VA facilities to determine the extent to which its findings are generalizable.

Acknowledgments
The authors thank Dr. Stevan Knezevich for reviewing cases, Pam Pehan for providing the list of VAPSHCS melanomas accessioned from VistA, and Eddie Alaniz and Eugene Gavrilenko for helping ascertain SNOMED codes.

Author disclosures
The authors report no actual or potential conflicts of interest with regard to this article.

Disclaimer
The opinions expressed herein are those of the authors and do not necessarily reflect those of Federal Practitioner, Frontline Medical Communications Inc., the U.S. Government, or any of its agencies. This article may discuss unlabeled or investigational use of certain drugs. Please review the complete prescribing information for specific drugs or drug combinations—including indications, contraindications, warnings, and adverse effects—before administering pharmacologic therapy to patients.

 

Click here to read the digital edition.

References

1. Division of Cancer Prevention and Control, Centers for Disease Control and Prevention. National Program of Cancer Registries (NPCR). CDC website. http://www.cdc.gov/cancer/npcr/about.htm. Updated April 20, 2016. Accessed July 1, 2016.

2. National Cancer Institute. Overview of the SEER program. National Cancer Institute website. http://seer.cancer.gov/about/overview.html. Accessed July 18, 2016.

3. Cancer Registries Amendment Act. 42 USC §201-280e (2016).

4. Cancer Registry of Greater California. Cancer reporting. Cancer Registry of Greater California website. http://crgc-cancer.org/hospitals-and-physicians. Accessed July 18, 2016.

5. American Academy of Dermatology. State cancer registry laws and requirements. American Academy of Dermatology website. https://www.aad.org/file%20library/global%20navigatio/education%20and%20quality%20care/state%20cancer%20registries/state-cancer-registries-laws-and-requirements.pdf. Accessed July 18, 2016.

6. Craig BM, Rollison DE, List AF, Cogle CR. Underreporting of myeloid malignancies by United States cancer registries. Cancer Epidemiol Biomarkers Prev. 2012;21(3):474-481.

7. Fanning J, Gangestad A, Andrews SJ. National Cancer Data Base/Surveillance Epidemiology and End Results: potential insensitive-measure bias. Gynecol Oncol. 2000;77(3):450-453.

8. Thoburn KK, German RR, Lewis M, Nichols PJ, Ahmed F, Jackson-Thompson J. Case completeness and data accuracy in the Centers for Disease Control and Prevention’s National Program of Cancer Registries. Cancer. 2007;109(8):1607-1616.

9. Cockburn M, Swetter SM, Peng D, Keegan TH, Deapen D, Clarke CA. Melanoma underreporting: why does it happen, how big is the problem, and how do we fix it? J Am Acad Dermatol. 2008;59(6):1081-1085.

10. Karagas MR, Thomas DB, Roth GJ, Johnson LK, Weiss NS. The effects of changes in health care delivery on the reported incidence of cutaneous melanoma in western Washington state. Am J Epidemiol. 1991;133(1):58-62.

11. Merlino LA, Sullivan KJ, Whitaker DC, Lynch CF. The independent pathology laboratory as a reporting source for cutaneous melanoma incidence in Iowa, 1977–1994. J Am Acad Dermatol. 1997;37(4):578-585.

12. Cartee TV, Kini SP, Chen SC. Melanoma reporting to central cancer registries by US dermatologists: an analysis of the persistent knowledge and practice gap. J Am Acad Dermatol. 2011;65(5)(suppl 1):S124-S132.

13. Clegg LX, Feuer EJ, Midthune DN, Fay MP, Hankey BF. Impact of reporting delay and reporting error on cancer incidence rates and trends. J Natl Cancer Inst. 2002;94(20):1537-1545.

14. Odds ratio calculator. MedCalc website. https://www.medcalc.org/calc/odds_ratio.php. Accessed June 16, 2016.

Note: Page numbers differ between the print issue and digital edition.

References

1. Division of Cancer Prevention and Control, Centers for Disease Control and Prevention. National Program of Cancer Registries (NPCR). CDC website. http://www.cdc.gov/cancer/npcr/about.htm. Updated April 20, 2016. Accessed July 1, 2016.

2. National Cancer Institute. Overview of the SEER program. National Cancer Institute website. http://seer.cancer.gov/about/overview.html. Accessed July 18, 2016.

3. Cancer Registries Amendment Act. 42 USC §201-280e (2016).

4. Cancer Registry of Greater California. Cancer reporting. Cancer Registry of Greater California website. http://crgc-cancer.org/hospitals-and-physicians. Accessed July 18, 2016.

5. American Academy of Dermatology. State cancer registry laws and requirements. American Academy of Dermatology website. https://www.aad.org/file%20library/global%20navigatio/education%20and%20quality%20care/state%20cancer%20registries/state-cancer-registries-laws-and-requirements.pdf. Accessed July 18, 2016.

6. Craig BM, Rollison DE, List AF, Cogle CR. Underreporting of myeloid malignancies by United States cancer registries. Cancer Epidemiol Biomarkers Prev. 2012;21(3):474-481.

7. Fanning J, Gangestad A, Andrews SJ. National Cancer Data Base/Surveillance Epidemiology and End Results: potential insensitive-measure bias. Gynecol Oncol. 2000;77(3):450-453.

8. Thoburn KK, German RR, Lewis M, Nichols PJ, Ahmed F, Jackson-Thompson J. Case completeness and data accuracy in the Centers for Disease Control and Prevention’s National Program of Cancer Registries. Cancer. 2007;109(8):1607-1616.

9. Cockburn M, Swetter SM, Peng D, Keegan TH, Deapen D, Clarke CA. Melanoma underreporting: why does it happen, how big is the problem, and how do we fix it? J Am Acad Dermatol. 2008;59(6):1081-1085.

10. Karagas MR, Thomas DB, Roth GJ, Johnson LK, Weiss NS. The effects of changes in health care delivery on the reported incidence of cutaneous melanoma in western Washington state. Am J Epidemiol. 1991;133(1):58-62.

11. Merlino LA, Sullivan KJ, Whitaker DC, Lynch CF. The independent pathology laboratory as a reporting source for cutaneous melanoma incidence in Iowa, 1977–1994. J Am Acad Dermatol. 1997;37(4):578-585.

12. Cartee TV, Kini SP, Chen SC. Melanoma reporting to central cancer registries by US dermatologists: an analysis of the persistent knowledge and practice gap. J Am Acad Dermatol. 2011;65(5)(suppl 1):S124-S132.

13. Clegg LX, Feuer EJ, Midthune DN, Fay MP, Hankey BF. Impact of reporting delay and reporting error on cancer incidence rates and trends. J Natl Cancer Inst. 2002;94(20):1537-1545.

14. Odds ratio calculator. MedCalc website. https://www.medcalc.org/calc/odds_ratio.php. Accessed June 16, 2016.

Note: Page numbers differ between the print issue and digital edition.

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Transplant recipients need dermatologists both pre- and post-transplant

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Boston – Shared medical appointments can work well for patients undergoing solid organ transplants and for the clinical staff treating them – serving as an efficient way to educate several patients in a common setting and giving them the opportunity to interact with others going through a similar experience.

“Having those shared medical appointments where they’re sitting next to somebody who’s going through the same thought process and information gathering ... and the ability to talk with similar folks is a huge benefit for those patients,” said Allison Vidimos, MD, chair of the department of dermatology at the Cleveland Clinic. Dr. Vidimos and her colleagues have been so focused on skin cancer diagnosis and treatment in this group of patients that “we’ve kind of lost sight of the human aspect of it and the fear that these patients have,” she added.

Dr. Allison Vidimos

These shared medical appointments at the Cleveland Clinic also provide the dermatology staff an efficient means to educate a group of patients about the risks of developing skin cancers and benign conditions associated with immunosuppressive treatments. They also discuss sun protection and avoidance practices, and how to perform skin self exams, all of which are “really important for their well being after their transplant,” Dr. Vidimos said during an interview at the American Academy of Dermatology summer meeting.

Patients learn how frequently they will need a clinical skin exam post-transplant, depending on the occurrence of skin cancers, and that biopsies may be necessary at times.

Dr. Vidimos said it is up to the transplant surgeons to discuss with patients the very low risk of transmission of malignancies from the donor to the recipient. In her presentation at the meeting, she cited a 1.4% risk of an undetected skin or internal malignancy in a donor being transmitted to the recipient.

Because of changes in criteria, patients who have relatively low risk skin cancers or higher risk skin cancers and have been treated, and are at “a defined interval post-treatment where we feel it’s safe to do that transplant,” may be considered a transplant candidate, she said noting that previously, such patients would be excluded from a transplant.

The appropriate time intervals to wait for a transplant for candidates with a history of cutaneous squamous cell carcinoma, malignant melanoma, or Merkel cell carcinoma are spelled out in a recently published consensus paper Dr. Vidimos coauthored with other members of the International Transplant Skin Cancer Collaborative (Am J Transplant. 2016 Feb;16[2]:407-13).

Dr. Vidimos said she is sometimes called to the bedside to perform a skin exam in a pretransplant patient who is very ill. The most common scenario is a liver transplant candidate awaiting transport to the operating room, who has not had a skin exam and needs to be cleared by a dermatologist to rule out a melanoma or another type of skin cancer that could be “fertilized” by postoperative immunosuppressant therapy.

After a transplant, patients need to be seen frequently enough to detect malignant transformation of precancerous skin lesions. Dermatologists should have a low threshold for biopsying any suspicious lesions early. “A lot of times we get biopsies back of skin cancer that do not match ... the clinical picture,” Dr. Vidimos said. Patients should be referred when the dermatologist feels that he or she can not deliver the appropriate treatment.

As transplants have become fairly routine and patients are living longer, community dermatologists will most likely be seeing solid organ transplant recipients more frequently. With longer lifespans, those patients will have more opportunity to develop more skin cancers.

Dr. Vidimos disclosed having received grants and research funding from Genentech.

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Boston – Shared medical appointments can work well for patients undergoing solid organ transplants and for the clinical staff treating them – serving as an efficient way to educate several patients in a common setting and giving them the opportunity to interact with others going through a similar experience.

“Having those shared medical appointments where they’re sitting next to somebody who’s going through the same thought process and information gathering ... and the ability to talk with similar folks is a huge benefit for those patients,” said Allison Vidimos, MD, chair of the department of dermatology at the Cleveland Clinic. Dr. Vidimos and her colleagues have been so focused on skin cancer diagnosis and treatment in this group of patients that “we’ve kind of lost sight of the human aspect of it and the fear that these patients have,” she added.

Dr. Allison Vidimos

These shared medical appointments at the Cleveland Clinic also provide the dermatology staff an efficient means to educate a group of patients about the risks of developing skin cancers and benign conditions associated with immunosuppressive treatments. They also discuss sun protection and avoidance practices, and how to perform skin self exams, all of which are “really important for their well being after their transplant,” Dr. Vidimos said during an interview at the American Academy of Dermatology summer meeting.

Patients learn how frequently they will need a clinical skin exam post-transplant, depending on the occurrence of skin cancers, and that biopsies may be necessary at times.

Dr. Vidimos said it is up to the transplant surgeons to discuss with patients the very low risk of transmission of malignancies from the donor to the recipient. In her presentation at the meeting, she cited a 1.4% risk of an undetected skin or internal malignancy in a donor being transmitted to the recipient.

Because of changes in criteria, patients who have relatively low risk skin cancers or higher risk skin cancers and have been treated, and are at “a defined interval post-treatment where we feel it’s safe to do that transplant,” may be considered a transplant candidate, she said noting that previously, such patients would be excluded from a transplant.

The appropriate time intervals to wait for a transplant for candidates with a history of cutaneous squamous cell carcinoma, malignant melanoma, or Merkel cell carcinoma are spelled out in a recently published consensus paper Dr. Vidimos coauthored with other members of the International Transplant Skin Cancer Collaborative (Am J Transplant. 2016 Feb;16[2]:407-13).

Dr. Vidimos said she is sometimes called to the bedside to perform a skin exam in a pretransplant patient who is very ill. The most common scenario is a liver transplant candidate awaiting transport to the operating room, who has not had a skin exam and needs to be cleared by a dermatologist to rule out a melanoma or another type of skin cancer that could be “fertilized” by postoperative immunosuppressant therapy.

After a transplant, patients need to be seen frequently enough to detect malignant transformation of precancerous skin lesions. Dermatologists should have a low threshold for biopsying any suspicious lesions early. “A lot of times we get biopsies back of skin cancer that do not match ... the clinical picture,” Dr. Vidimos said. Patients should be referred when the dermatologist feels that he or she can not deliver the appropriate treatment.

As transplants have become fairly routine and patients are living longer, community dermatologists will most likely be seeing solid organ transplant recipients more frequently. With longer lifespans, those patients will have more opportunity to develop more skin cancers.

Dr. Vidimos disclosed having received grants and research funding from Genentech.

Boston – Shared medical appointments can work well for patients undergoing solid organ transplants and for the clinical staff treating them – serving as an efficient way to educate several patients in a common setting and giving them the opportunity to interact with others going through a similar experience.

“Having those shared medical appointments where they’re sitting next to somebody who’s going through the same thought process and information gathering ... and the ability to talk with similar folks is a huge benefit for those patients,” said Allison Vidimos, MD, chair of the department of dermatology at the Cleveland Clinic. Dr. Vidimos and her colleagues have been so focused on skin cancer diagnosis and treatment in this group of patients that “we’ve kind of lost sight of the human aspect of it and the fear that these patients have,” she added.

Dr. Allison Vidimos

These shared medical appointments at the Cleveland Clinic also provide the dermatology staff an efficient means to educate a group of patients about the risks of developing skin cancers and benign conditions associated with immunosuppressive treatments. They also discuss sun protection and avoidance practices, and how to perform skin self exams, all of which are “really important for their well being after their transplant,” Dr. Vidimos said during an interview at the American Academy of Dermatology summer meeting.

Patients learn how frequently they will need a clinical skin exam post-transplant, depending on the occurrence of skin cancers, and that biopsies may be necessary at times.

Dr. Vidimos said it is up to the transplant surgeons to discuss with patients the very low risk of transmission of malignancies from the donor to the recipient. In her presentation at the meeting, she cited a 1.4% risk of an undetected skin or internal malignancy in a donor being transmitted to the recipient.

Because of changes in criteria, patients who have relatively low risk skin cancers or higher risk skin cancers and have been treated, and are at “a defined interval post-treatment where we feel it’s safe to do that transplant,” may be considered a transplant candidate, she said noting that previously, such patients would be excluded from a transplant.

The appropriate time intervals to wait for a transplant for candidates with a history of cutaneous squamous cell carcinoma, malignant melanoma, or Merkel cell carcinoma are spelled out in a recently published consensus paper Dr. Vidimos coauthored with other members of the International Transplant Skin Cancer Collaborative (Am J Transplant. 2016 Feb;16[2]:407-13).

Dr. Vidimos said she is sometimes called to the bedside to perform a skin exam in a pretransplant patient who is very ill. The most common scenario is a liver transplant candidate awaiting transport to the operating room, who has not had a skin exam and needs to be cleared by a dermatologist to rule out a melanoma or another type of skin cancer that could be “fertilized” by postoperative immunosuppressant therapy.

After a transplant, patients need to be seen frequently enough to detect malignant transformation of precancerous skin lesions. Dermatologists should have a low threshold for biopsying any suspicious lesions early. “A lot of times we get biopsies back of skin cancer that do not match ... the clinical picture,” Dr. Vidimos said. Patients should be referred when the dermatologist feels that he or she can not deliver the appropriate treatment.

As transplants have become fairly routine and patients are living longer, community dermatologists will most likely be seeing solid organ transplant recipients more frequently. With longer lifespans, those patients will have more opportunity to develop more skin cancers.

Dr. Vidimos disclosed having received grants and research funding from Genentech.

References

References

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Effectiveness of an Employee Skin Cancer Screening Program for Secondary Prevention

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Effectiveness of an Employee Skin Cancer Screening Program for Secondary Prevention

The incidence of skin cancer, along with its effects on patients and the economy, has continued to increase and therefore requires particular attention from dermatologists. UV light has been shown to be of etiopathologic importance in the development of various types of skin cancer.1-3 Studies have shown that there is a direct correlation between the incidence of skin cancer and average annual amounts of UV radiation exposure.3 Accordingly, in 2009 the International Agency for Research on Cancer classified UV light as carcinogenic to humans.4 Therefore, the general public must be made aware of the danger of exposure to UV radiation.

In Australia, government initiatives to educate the population on causes of skin cancer development and its relationship to UV radiation have already caused the public to change their way of thinking and to deal with sunlight in a conscious and responsible manner.5 A large proportion of the Australian population with light skin is at a particularly high risk for developing skin cancer due to intense exposure to UV radiation. Numerous campaigns in Germany and other countries have attempted to sensitize the public to this issue by emphasizing a reduction in UV exposure (primary prevention) or highlighting the importance of early diagnosis (secondary prevention).6,7

For a good prognosis, it is crucial that skin cancer, particularly melanoma, is discovered at an early or precancerous stage.8 For this reason, self-examination of the skin and skin cancer screening are important factors that can contribute to ensuring early and curative treatment.9-11 Since July 1, 2008, skin cancer screenings have been included in the preventative health care program by statutory health insurance providers in Germany. As part of this program, the cost of screening once every 2 years for individuals 35 years and older is covered by statutory health insurance.12 Several studies have shown a decline in the melanoma mortality rate since the introduction of skin cancer screening programs in Germany.11,13,14

Employee skin cancer screening programs are an important method of examining high numbers of individuals quickly and effectively. These programs have been carried out in Germany and other countries.15,16 Studies have shown that skin cancer screening carried out selectively on defined groups can be an effective form of secondary prevention, particularly for those who work outdoors.17

An employee skin cancer screening program was carried out as part of this study. The findings are interpreted and discussed in relation to other employee screening programs that have been reported as well as those introduced by statutory health insurance providers in Germany. The aim of this study was to determine the importance and effectiveness of employee skin cancer screening programs and the role they play in secondary prevention of skin cancer.

Methods

Study Population

Employees of a technical company in Bavaria, Germany, were offered a skin cancer screening program by the employer’s occupational health service and health insurance provider in collaboration with the Department of Dermatology at the University Hospital Erlangen (Erlangen, Germany). Skin examinations were performed exclusively by 5 trained dermatologists. Only direct employees of the company at 3 of its locations in the Erlangen area were eligible to participate. The total number of employees varied by location (1072–5126 employees). The majority of employees had a university education or had completed technical training. Family members and other individuals who were not members of the company were excluded. There were no further inclusion or exclusion criteria. Over a period of 13 days, 783 of 7823 total employees (10.0%) were examined and included in the study. The study was approved by the Responsible Ethics Commission of the Faculty of Medicine at Friedrich-Alexander-University Erlangen-Nürnberg, Germany.

 

 

Study Design

Employees signed a consent form for participation in the study and completed a standardized questionnaire. The questionnaire was based on surveys used in a prior study18 and collected information on current and prior skin lesions, prior dermatological screening, personal and family history of skin tumors, frequency of UV exposure, and type of UV protection used. For the question on measures taken for protection from UV radiation, possible answers included with sunscreen cream, with suitable sun-protective clothing, and by staying in the shade, or no measures were taken. In contrast to the other questions, multiple answers were accepted for this question. Answering no automatically excluded other possible answers. Participants also were asked to assess their own Fitzpatrick skin type19; the questionnaire included explanations of each skin type (I–IV).

The participants were then called in for examination by the dermatologist at 15-minute intervals. All clothing was removed and the skin was examined. Dermatoscopes were used for closer examination of suspicious skin lesions. The clinical results of the examinations were recorded on a standardized form.

An estimation of the number of melanocytic nevi—≤20, 21–49, or ≥50—was recorded for each patient. Suspicious skin lesions were assigned to one of the following categories: nevus requiring future checkup (Nc), nevus requiring excision (Ne), suspected malignant melanoma (MM), suspected squamous cell carcinoma, suspected basal cell carcinoma (BCC), suspected other skin tumor, and precancerous lesion. Fitzpatrick skin type also was assessed for all participants and recorded by the dermatologist carrying out the examination. Each participant was assigned to a risk group—low, moderate, or high risk—based on their individual risk for developing a skin tumor. Factors that were considered when determining participants’ risk for developing skin cancer included Fitzpatrick skin type, number of melanocytic nevi, personal and family history, leisure activities, UV protection used, and current clinical diagnosis of skin lesions.

After the skin examination, participants were informed of recommended treatment but were not given any additional dermatologic advice. Participants could arrange an appointment at the Department of Dermatology, University Hospital Erlangen, for the excision and histological analysis of the skin lesions. All recorded data were collected in a computerized spreadsheet program. When evaluating the questionnaires, questions that were not answered or were answered incorrectly (participant chose more than 1 answer) were ignored.

Statistical Analysis

Statistical analysis was carried out using SPSS software version 16.0. The majority of the data were nominal or ordinal. Metric data were checked for normal distribution using the Shapiro-Wilk test before carrying out parametric tests. Statistical tests were carried out using the χ2 test and the t test for independent samples. Non-nominal distributed data were checked using the Mann-Whitney U test. P<.05 was considered statistically significant in the exploratory data analysis.

Results

Of 783 employees included in the study, 288 (36.8%) were female and 495 (63.2%) were male (Table 1). In comparison with the total workforce, a significantly higher proportion of women than men took part in the cross-sectional study (P<.01). The average age (SD) was 42.3 (9.5) years (range, 18–64 years). Female participants (average age [SD], 39.8 [10.2] years) were significantly younger than male participants (average age [SD], 43.8 [8.8] years; P<.01). Forty-one percent of participants had a prior skin cancer screening. One percent of participants had a personal history of skin cancer, with 1 participant reporting a history of MM; 6.5% had a family history of skin cancer, of which 39.2% had a family history of MM.

The results of the clinical examinations showed that 43.8% of participants had 20 or fewer melanocytic nevi, 43.4% had 21 to 49 melanocytic nevi, and 12.8% had 50 or more melanocytic nevi. Significantly more women than men had 20 or fewer melanocytic nevi (P<.05).

Approximately 92% of participants assessed themselves as having Fitzpatrick skin types II (35.2%) or III (56.7%), while only approximately 3.6% and 4.5% assessed themselves as having skin types I and IV, respectively. The results of the Fitzpatrick skin type assessments made by dermatologists were similar: 96.9% of participants were assessed as having Fitzpatrick skin types II (43.0%) and III (53.8%); approximately 1.9% and 1.3% were assessed as having Fitzpatrick skin types I and IV, respectively. Results showed that 80.2% of all participants assessed their skin type in the same way as the dermatologist; 13.5% assessed their skin type as darker and 6.3% (49/783) assessed it as lighter. A quantitative analysis of Fitzpatrick skin type and sex showed that significantly more male participants than female participants assessed their Fitzpatrick skin type darker than their actual skin type (P<.01).

Overall, 47.6% of participants reported having had sunburn rarely in the past, while 36.9% and 14.0% had experienced sunburn once per year and several times per year, respectively. Approximately 1.4% of participants reported never having a sunburn. More of the male participants made use of comprehensive sun protection using all methods listed (34.5%; P<.05) or a combination of sunscreen and sun-protective clothing (14.9%; P<.01) than the female participants who relied more frequently on sunscreen alone (29.5%; P<.01) or a combination of sunscreen and staying in the shade (29.5%; P<.01)

In general it was clear that sunscreen, either alone or in combination with other sun-protection methods, was used most frequently (88.0%); 58.0% protected themselves by staying in the shade, while 48.0% used suitable sun-protective clothing. Only 3.6% of participants did not protect themselves using any of the suggested methods.

A total of 661 categorized skin lesions were found in 377 participants. Of these lesions, 491 were Nc and 121 were Ne. Twenty-four of the skin lesions were suspected precancerous lesions, 13 were suspected BCC, 2 were suspected MM, and 10 were suspected other skin tumor (Table 2). Overall, male participants who were diagnosed with at least 1 skin lesion (average age, 44.0 years) were significantly older than the women (average age, 39.3 years)(P<.01). Similar findings were observed in participants with at least 1 Nc (men, 43.3 years; women, 38.7 years; P<.01) and at least 1 Ne (men, 44.2 years; women, 38.0 years; P<.05). With regard to the individual risk for developing skin cancer, 32.6% of participants were considered to be at low risk, 64.9% were at moderate risk, and 2.6% were at high risk.

Approximately 61.5% of 377 participants who were diagnosed with at least 1 categorized skin lesion were advised to have a specific skin lesion checked by a dermatologist or to have a full examination for skin cancer once every 12 months. Furthermore, 22.5% were advised to follow-up biannually and 11.7% were advised to follow-up once every 2 years. Of the remaining participants who were advised to have follow-ups, 0.3% were advised to have a skin examination once every 3 months after having had MM, and 4.0% were advised to have follow-up once every 18 months. Overall, follow-up was recommended within 1 year in 84.4% of cases and within 1 to 2 years in 15.6% (Table 3).

Subsequent histological analysis of the excised tissue resulted in a diagnosis of only 21 clinically significant skin conditions. One case of Bowen disease and 1 case of BCC was confirmed. Histological analysis identified the remaining 19 excised skin lesions, which included the 2 suspected MMs, as dysplastic nevi.

 

 

Comment

The aim of this cross-sectional study was to examine the importance and effectiveness of employee skin cancer screening programs. In comparison with the total workforce, significantly more women took part than men. Female participants were significantly younger than male participants, which mirrors the findings of prior studies showing that screening programs reach women more frequently than men and that women who participate in screenings are also younger on average in comparison to men.7-13 Men and older individuals usually are underrepresented.7,13 The average age of participants in our study was 42.3 years, which is lower than in the SCREEN (Skin Cancer Research to Provide Evidence for Effectiveness of Screening in Northern Germany) study (average age, 49.7 years).13 The average age in our study also is likely to be lower than patients who undergo skin cancer screenings offered by statutory health insurance providers in Germany, which has a minimum age restriction of 35 years; however, it is comparable to the average age of participants in other employee screening programs and therefore represents the average age of individuals employed in Germany.15,16

The employee skin cancer screening program in this study generated a high level of interest, indicated by the fact that all available appointments had been booked just 36 hours after the screening was announced. Furthermore, there was a waiting list of approximately 300 employees who were not able to undergo a skin examination. For logistical reasons, the number of participants was limited to 10% of the workforce. The high level of interest is an indication of increased awareness of the importance of recognizing skin tumors early and the associated need for information as well as the need to undergo screening for skin cancer as a precaution. This observation also can be made with regard to the skin cancer screening introduced by statutory health insurance providers in Germany. Studies published by Augustin et al20 and Kornek et al21,22 confirm that skin cancer screenings have gained wide acceptance in Germany because they were introduced by statutory health insurance providers in 2008. The number of skin cancer screenings carried out by dermatologists in Germany also is increasing.20-22 Although approximately 19% of those eligible to participate took part in the SCREEN pilot project,13 approximately 31% of individuals who were eligible to participate took part in skin cancer screenings offered by statutory health insurance providers in Germany in 2012, and the percentage is rising.23 Two important factors affecting the high level of interest in the employee screening program used in our study were undoubtedly the advantages of the examination taking place during working hours and being held on the occupational health services’ premises in the workplace, which helped participants avoid the cost of travel and wait times associated with visiting a medical practice.

Of 783 participants included in this study, 377 displayed at least 1 categorized skin lesion; the majority were suspicious melanocytic nevi. This high incidence rate suggested that regular skin cancer screenings are useful, as it has been shown that there is a correlation between higher numbers of melanocytic nevi and increased risk for developing melanoma.24

In a study by Winkler et al,25 a skin cancer screening of 1658 bank and insurance employees found that 33.8% of those examined displayed at least 1 atypical melanocytic nevus and 27.2% displayed more than 50 melanocytic nevi (compared to 12.8% with ≥50 melanocytic nevi in the current study). The risk for developing skin cancer was classified as intermediate or high in 54.5% (compared to 67.5% at moderate or high risk in the current study).25 Therefore, the rate of suspicious skin lesions was lower in the population of the study by Winkler et al25 in comparison to the population of the current study. As the overall number of melanocytic nevi and the individual risk for skin cancer, however, was underestimated by the majority of the bank and insurance employees,25 employee skin cancer screening programs can be used as a potentially effective tool to make employees aware of the issue and sensitizing them to it. Employee screening in addition to a final diagnosis can contribute to ensuring suitable treatment is started. For example, in the large-scale employee screening published by Schaefer et al15 and Augustin et al,16 48,665 and 90,880 employees, respectively, were screened for inflammatory and noninflammatory skin diseases, and 19% and 27% of participants, respectively, were diagnosed with skin lesions that required treatment.

Participants in the current study were given no further treatment or advice. Recommendations were made that participants monitor suspicious skin lesions or have them removed. With regard to future screening, 84.4% of participants with at least 1 categorized skin lesion were advised to have a regular follow-up within 1 year, while 15.6% were advised to follow-up within 1 to 2 years. Therefore, a period of 2 years before the next checkup, the period between screenings offered by statutory health insurance providers in Germany,12 was considered too long for the majority of participants, according to the dermatologists involved with our study.

Conclusion

The high rate of suspicious skin lesions diagnosed demonstrated the effectiveness of skin cancer screenings organized in the workplace, which should be recommended for all employees, not only those who are at high risk for developing skin cancer due to the nature of their work, such as those who work outdoors. It should be noted that the study group examined in the current study was a homogeneous group of employees of a technical company only and is therefore relatively selective. Nevertheless, despite the comparatively selective and young participant group, these examinations provide evidence of the importance of skin cancer screening programs for a wider population.

Acknowledgments

The authors thank Heidi Seybold, MD; Petra Wörl, MD; Sybille Thoma-Uszynski, MD; and Jens Bussmann, MD (all from Erlangen, Germany), for their support and active assistance in the practical implementation of this study.

References
  1. Boniol M, Autier P, Boyle P, et al. Cutaneous melanoma attributable to sunbed use: systematic review and meta-analysis. BMJ. 2012;345:e4757.
  2. Gilchrest BA, Eller MS, Geller AC, et al. The pathogenesis of melanoma induced by ultraviolet radiation. N Engl J Med. 1999;340:1341-1348.
  3. Rigel DS. Cutaneous ultraviolet exposure and its relationship to the development of skin cancer. J Am Acad Dermatol. 2008;58:129-132.
  4. El Ghissassi F, Baan R, Straif K, et al; WHO International Agency for Research on Cancer Monograph Working Group. A review of human carcinogens—part D: radiation. Lancet Oncol. 2009;10:751-752.
  5. MacLennan R, Green AC, McLeod GR, et al. Increasing incidence of cutaneous melanoma in Queensland, Australia. J Natl Cancer Inst. 1992;84:1427-1432.
  6. Heinzerling LM, Dummer R, Panizzon RG, et al. Prevention campaign against skin cancer. Dermatology. 2002;205:229-233.
  7. Stratigos A, Nikolaou V, Kedicoglou S, et al. Melanoma/skin cancer screening in a Mediterranean country: results of the Euromelanoma Screening Day Campaign in Greece. J Eur Acad Dermatol Venereol. 2007;21:56-62.
  8. Garbe C, Hauschild A, Volkenandt M, et al. Evidence and interdisciplinary consense-based German guidelines: diagnosis and surveillance of melanoma. Melanoma Res. 2007;17:393-399.
  9. Choudhury K, Volkmer B, Greinert R, et al. Effectiveness of skin cancer screening programmes. Br J Dermatol. 2012;167:94-98.
  10. Eisemann N, Waldmann A, Geller AC, et al. Non-melanoma skin cancer incidence and impact of skin cancer screening on incidence. J Invest Dermatol. 2014;134:43-50.
  11. Katalinic A, Waldmann A, Weinstock MA, et al. Does skin cancer screening save lives? an observational study comparing trends in melanoma mortality in regions with and without screening. Cancer. 2012;118:5395-5402.
  12. Bekanntmachung (1430 A) eines Beschlusses des Gemeinsamen Bundeausschusses über eine Änderung der Krebsfrüherkennungs-Richtlinien: Hautkrebs-Screening [press release]. Berlin, Germany: Bundesministerium für Gesundheit (Federal Ministry of Health, Germany); vom 15. November 2007.
  13. Breitbart EW, Waldmann A, Nolte S, et al. Systematic skin cancer screening in Northern Germany. J Am Acad Dermatol. 2012;66:201-211.
  14. Waldmann A, Nolte S, Weinstock MA, et al. Skin cancer screening participation and impact on melanoma incidence in Germany—an observational study on incidence trends in regions with and without population-based screening. Br J Cancer. 2012;106:970-974.
  15. Schaefer I, Rustenbach SJ, Zimmer L, et al. Prevalence of skin diseases in a cohort of 48,665 employees in Germany. Dermatology. 2008;217:169-172.
  16. Augustin M, Herberger K, Hintzen S, et al. Prevalence of skin lesions and need for treatment in a cohort of 90880 workers. Br J Dermatol. 2011;165:865-873.
  17. LeBlanc WG, Vidal L, Kirsner RS, et al. Reported skin cancer screening of US adult workers. J Am Acad Dermatol. 2008;59:55-63.
  18. Harbauer A, Binder M, Pehamberger H, et al. Validity of an unsupervised self-administered questionnaire for self-assessment of melanoma risk. Melanoma Res. 2003;13:537-542.
  19. Fitzpatrick TB. The validity and practicality of sun-reactive skin types I through VI. Arch Dermatol. 1988;124:869-871.
  20. Augustin M, Stadler R, Reusch M, et al. Skin cancer screening in Germany—perception by the public. J Dtsch Dermatol Ges. 2012;10:42-49.
  21. Kornek T, Augustin M. Skin cancer prevention. J Dtsch Dermatol Ges. 2013;11:283-296.
  22. Kornek T, Schäfer I, Reusch M, et al. Routine skin cancer screening in Germany: four years of experience from the dermatologists’ perspective. Dermatology. 2012;225:289-293.
  23. Barmer GEK Arztreport 2014 [press release]. Berlin, Germany: Barmer GEK; February 4, 2014.
  24. Bauer J, Garbe C. Acquired melanocytic nevi as riskfactor for melanoma development. a comprehensive review of epidemiological data. Pigment Cell Res. 2003;16:297-306.
  25. Winkler A, Plugfelder A, Weide B, et al. Screening for skin cancer in bank and insurance employees: risk profile and correlation of self and physician’s assessment. Int J Dermatol. 2015;54:419-423.
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Drs. Uslu, Uter, and Sticherling are from the Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Univeristätsklinikum Erlangen, Germany. Drs. Uslu and Sticherling are from the Department of Dermatology, and Dr. Uter is from the Department of Medical Informatics, Biometry and Epidemiology. Dr. Hees is from the Department of Otorhinolaryngology, Nürnberg Hospital North, Germany. Dr. Winnik is from Siemens Healthcare GmbH, Erlangen.

The authors report no conflict of interest.

Correspondence: Ugur Uslu, MD, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Department of Dermatology, Univeristätsklinikum Erlangen, Ulmenweg 18, D-91054 Erlangen, Germany ([email protected]).

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Drs. Uslu, Uter, and Sticherling are from the Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Univeristätsklinikum Erlangen, Germany. Drs. Uslu and Sticherling are from the Department of Dermatology, and Dr. Uter is from the Department of Medical Informatics, Biometry and Epidemiology. Dr. Hees is from the Department of Otorhinolaryngology, Nürnberg Hospital North, Germany. Dr. Winnik is from Siemens Healthcare GmbH, Erlangen.

The authors report no conflict of interest.

Correspondence: Ugur Uslu, MD, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Department of Dermatology, Univeristätsklinikum Erlangen, Ulmenweg 18, D-91054 Erlangen, Germany ([email protected]).

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Drs. Uslu, Uter, and Sticherling are from the Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Univeristätsklinikum Erlangen, Germany. Drs. Uslu and Sticherling are from the Department of Dermatology, and Dr. Uter is from the Department of Medical Informatics, Biometry and Epidemiology. Dr. Hees is from the Department of Otorhinolaryngology, Nürnberg Hospital North, Germany. Dr. Winnik is from Siemens Healthcare GmbH, Erlangen.

The authors report no conflict of interest.

Correspondence: Ugur Uslu, MD, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Department of Dermatology, Univeristätsklinikum Erlangen, Ulmenweg 18, D-91054 Erlangen, Germany ([email protected]).

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The incidence of skin cancer, along with its effects on patients and the economy, has continued to increase and therefore requires particular attention from dermatologists. UV light has been shown to be of etiopathologic importance in the development of various types of skin cancer.1-3 Studies have shown that there is a direct correlation between the incidence of skin cancer and average annual amounts of UV radiation exposure.3 Accordingly, in 2009 the International Agency for Research on Cancer classified UV light as carcinogenic to humans.4 Therefore, the general public must be made aware of the danger of exposure to UV radiation.

In Australia, government initiatives to educate the population on causes of skin cancer development and its relationship to UV radiation have already caused the public to change their way of thinking and to deal with sunlight in a conscious and responsible manner.5 A large proportion of the Australian population with light skin is at a particularly high risk for developing skin cancer due to intense exposure to UV radiation. Numerous campaigns in Germany and other countries have attempted to sensitize the public to this issue by emphasizing a reduction in UV exposure (primary prevention) or highlighting the importance of early diagnosis (secondary prevention).6,7

For a good prognosis, it is crucial that skin cancer, particularly melanoma, is discovered at an early or precancerous stage.8 For this reason, self-examination of the skin and skin cancer screening are important factors that can contribute to ensuring early and curative treatment.9-11 Since July 1, 2008, skin cancer screenings have been included in the preventative health care program by statutory health insurance providers in Germany. As part of this program, the cost of screening once every 2 years for individuals 35 years and older is covered by statutory health insurance.12 Several studies have shown a decline in the melanoma mortality rate since the introduction of skin cancer screening programs in Germany.11,13,14

Employee skin cancer screening programs are an important method of examining high numbers of individuals quickly and effectively. These programs have been carried out in Germany and other countries.15,16 Studies have shown that skin cancer screening carried out selectively on defined groups can be an effective form of secondary prevention, particularly for those who work outdoors.17

An employee skin cancer screening program was carried out as part of this study. The findings are interpreted and discussed in relation to other employee screening programs that have been reported as well as those introduced by statutory health insurance providers in Germany. The aim of this study was to determine the importance and effectiveness of employee skin cancer screening programs and the role they play in secondary prevention of skin cancer.

Methods

Study Population

Employees of a technical company in Bavaria, Germany, were offered a skin cancer screening program by the employer’s occupational health service and health insurance provider in collaboration with the Department of Dermatology at the University Hospital Erlangen (Erlangen, Germany). Skin examinations were performed exclusively by 5 trained dermatologists. Only direct employees of the company at 3 of its locations in the Erlangen area were eligible to participate. The total number of employees varied by location (1072–5126 employees). The majority of employees had a university education or had completed technical training. Family members and other individuals who were not members of the company were excluded. There were no further inclusion or exclusion criteria. Over a period of 13 days, 783 of 7823 total employees (10.0%) were examined and included in the study. The study was approved by the Responsible Ethics Commission of the Faculty of Medicine at Friedrich-Alexander-University Erlangen-Nürnberg, Germany.

 

 

Study Design

Employees signed a consent form for participation in the study and completed a standardized questionnaire. The questionnaire was based on surveys used in a prior study18 and collected information on current and prior skin lesions, prior dermatological screening, personal and family history of skin tumors, frequency of UV exposure, and type of UV protection used. For the question on measures taken for protection from UV radiation, possible answers included with sunscreen cream, with suitable sun-protective clothing, and by staying in the shade, or no measures were taken. In contrast to the other questions, multiple answers were accepted for this question. Answering no automatically excluded other possible answers. Participants also were asked to assess their own Fitzpatrick skin type19; the questionnaire included explanations of each skin type (I–IV).

The participants were then called in for examination by the dermatologist at 15-minute intervals. All clothing was removed and the skin was examined. Dermatoscopes were used for closer examination of suspicious skin lesions. The clinical results of the examinations were recorded on a standardized form.

An estimation of the number of melanocytic nevi—≤20, 21–49, or ≥50—was recorded for each patient. Suspicious skin lesions were assigned to one of the following categories: nevus requiring future checkup (Nc), nevus requiring excision (Ne), suspected malignant melanoma (MM), suspected squamous cell carcinoma, suspected basal cell carcinoma (BCC), suspected other skin tumor, and precancerous lesion. Fitzpatrick skin type also was assessed for all participants and recorded by the dermatologist carrying out the examination. Each participant was assigned to a risk group—low, moderate, or high risk—based on their individual risk for developing a skin tumor. Factors that were considered when determining participants’ risk for developing skin cancer included Fitzpatrick skin type, number of melanocytic nevi, personal and family history, leisure activities, UV protection used, and current clinical diagnosis of skin lesions.

After the skin examination, participants were informed of recommended treatment but were not given any additional dermatologic advice. Participants could arrange an appointment at the Department of Dermatology, University Hospital Erlangen, for the excision and histological analysis of the skin lesions. All recorded data were collected in a computerized spreadsheet program. When evaluating the questionnaires, questions that were not answered or were answered incorrectly (participant chose more than 1 answer) were ignored.

Statistical Analysis

Statistical analysis was carried out using SPSS software version 16.0. The majority of the data were nominal or ordinal. Metric data were checked for normal distribution using the Shapiro-Wilk test before carrying out parametric tests. Statistical tests were carried out using the χ2 test and the t test for independent samples. Non-nominal distributed data were checked using the Mann-Whitney U test. P<.05 was considered statistically significant in the exploratory data analysis.

Results

Of 783 employees included in the study, 288 (36.8%) were female and 495 (63.2%) were male (Table 1). In comparison with the total workforce, a significantly higher proportion of women than men took part in the cross-sectional study (P<.01). The average age (SD) was 42.3 (9.5) years (range, 18–64 years). Female participants (average age [SD], 39.8 [10.2] years) were significantly younger than male participants (average age [SD], 43.8 [8.8] years; P<.01). Forty-one percent of participants had a prior skin cancer screening. One percent of participants had a personal history of skin cancer, with 1 participant reporting a history of MM; 6.5% had a family history of skin cancer, of which 39.2% had a family history of MM.

The results of the clinical examinations showed that 43.8% of participants had 20 or fewer melanocytic nevi, 43.4% had 21 to 49 melanocytic nevi, and 12.8% had 50 or more melanocytic nevi. Significantly more women than men had 20 or fewer melanocytic nevi (P<.05).

Approximately 92% of participants assessed themselves as having Fitzpatrick skin types II (35.2%) or III (56.7%), while only approximately 3.6% and 4.5% assessed themselves as having skin types I and IV, respectively. The results of the Fitzpatrick skin type assessments made by dermatologists were similar: 96.9% of participants were assessed as having Fitzpatrick skin types II (43.0%) and III (53.8%); approximately 1.9% and 1.3% were assessed as having Fitzpatrick skin types I and IV, respectively. Results showed that 80.2% of all participants assessed their skin type in the same way as the dermatologist; 13.5% assessed their skin type as darker and 6.3% (49/783) assessed it as lighter. A quantitative analysis of Fitzpatrick skin type and sex showed that significantly more male participants than female participants assessed their Fitzpatrick skin type darker than their actual skin type (P<.01).

Overall, 47.6% of participants reported having had sunburn rarely in the past, while 36.9% and 14.0% had experienced sunburn once per year and several times per year, respectively. Approximately 1.4% of participants reported never having a sunburn. More of the male participants made use of comprehensive sun protection using all methods listed (34.5%; P<.05) or a combination of sunscreen and sun-protective clothing (14.9%; P<.01) than the female participants who relied more frequently on sunscreen alone (29.5%; P<.01) or a combination of sunscreen and staying in the shade (29.5%; P<.01)

In general it was clear that sunscreen, either alone or in combination with other sun-protection methods, was used most frequently (88.0%); 58.0% protected themselves by staying in the shade, while 48.0% used suitable sun-protective clothing. Only 3.6% of participants did not protect themselves using any of the suggested methods.

A total of 661 categorized skin lesions were found in 377 participants. Of these lesions, 491 were Nc and 121 were Ne. Twenty-four of the skin lesions were suspected precancerous lesions, 13 were suspected BCC, 2 were suspected MM, and 10 were suspected other skin tumor (Table 2). Overall, male participants who were diagnosed with at least 1 skin lesion (average age, 44.0 years) were significantly older than the women (average age, 39.3 years)(P<.01). Similar findings were observed in participants with at least 1 Nc (men, 43.3 years; women, 38.7 years; P<.01) and at least 1 Ne (men, 44.2 years; women, 38.0 years; P<.05). With regard to the individual risk for developing skin cancer, 32.6% of participants were considered to be at low risk, 64.9% were at moderate risk, and 2.6% were at high risk.

Approximately 61.5% of 377 participants who were diagnosed with at least 1 categorized skin lesion were advised to have a specific skin lesion checked by a dermatologist or to have a full examination for skin cancer once every 12 months. Furthermore, 22.5% were advised to follow-up biannually and 11.7% were advised to follow-up once every 2 years. Of the remaining participants who were advised to have follow-ups, 0.3% were advised to have a skin examination once every 3 months after having had MM, and 4.0% were advised to have follow-up once every 18 months. Overall, follow-up was recommended within 1 year in 84.4% of cases and within 1 to 2 years in 15.6% (Table 3).

Subsequent histological analysis of the excised tissue resulted in a diagnosis of only 21 clinically significant skin conditions. One case of Bowen disease and 1 case of BCC was confirmed. Histological analysis identified the remaining 19 excised skin lesions, which included the 2 suspected MMs, as dysplastic nevi.

 

 

Comment

The aim of this cross-sectional study was to examine the importance and effectiveness of employee skin cancer screening programs. In comparison with the total workforce, significantly more women took part than men. Female participants were significantly younger than male participants, which mirrors the findings of prior studies showing that screening programs reach women more frequently than men and that women who participate in screenings are also younger on average in comparison to men.7-13 Men and older individuals usually are underrepresented.7,13 The average age of participants in our study was 42.3 years, which is lower than in the SCREEN (Skin Cancer Research to Provide Evidence for Effectiveness of Screening in Northern Germany) study (average age, 49.7 years).13 The average age in our study also is likely to be lower than patients who undergo skin cancer screenings offered by statutory health insurance providers in Germany, which has a minimum age restriction of 35 years; however, it is comparable to the average age of participants in other employee screening programs and therefore represents the average age of individuals employed in Germany.15,16

The employee skin cancer screening program in this study generated a high level of interest, indicated by the fact that all available appointments had been booked just 36 hours after the screening was announced. Furthermore, there was a waiting list of approximately 300 employees who were not able to undergo a skin examination. For logistical reasons, the number of participants was limited to 10% of the workforce. The high level of interest is an indication of increased awareness of the importance of recognizing skin tumors early and the associated need for information as well as the need to undergo screening for skin cancer as a precaution. This observation also can be made with regard to the skin cancer screening introduced by statutory health insurance providers in Germany. Studies published by Augustin et al20 and Kornek et al21,22 confirm that skin cancer screenings have gained wide acceptance in Germany because they were introduced by statutory health insurance providers in 2008. The number of skin cancer screenings carried out by dermatologists in Germany also is increasing.20-22 Although approximately 19% of those eligible to participate took part in the SCREEN pilot project,13 approximately 31% of individuals who were eligible to participate took part in skin cancer screenings offered by statutory health insurance providers in Germany in 2012, and the percentage is rising.23 Two important factors affecting the high level of interest in the employee screening program used in our study were undoubtedly the advantages of the examination taking place during working hours and being held on the occupational health services’ premises in the workplace, which helped participants avoid the cost of travel and wait times associated with visiting a medical practice.

Of 783 participants included in this study, 377 displayed at least 1 categorized skin lesion; the majority were suspicious melanocytic nevi. This high incidence rate suggested that regular skin cancer screenings are useful, as it has been shown that there is a correlation between higher numbers of melanocytic nevi and increased risk for developing melanoma.24

In a study by Winkler et al,25 a skin cancer screening of 1658 bank and insurance employees found that 33.8% of those examined displayed at least 1 atypical melanocytic nevus and 27.2% displayed more than 50 melanocytic nevi (compared to 12.8% with ≥50 melanocytic nevi in the current study). The risk for developing skin cancer was classified as intermediate or high in 54.5% (compared to 67.5% at moderate or high risk in the current study).25 Therefore, the rate of suspicious skin lesions was lower in the population of the study by Winkler et al25 in comparison to the population of the current study. As the overall number of melanocytic nevi and the individual risk for skin cancer, however, was underestimated by the majority of the bank and insurance employees,25 employee skin cancer screening programs can be used as a potentially effective tool to make employees aware of the issue and sensitizing them to it. Employee screening in addition to a final diagnosis can contribute to ensuring suitable treatment is started. For example, in the large-scale employee screening published by Schaefer et al15 and Augustin et al,16 48,665 and 90,880 employees, respectively, were screened for inflammatory and noninflammatory skin diseases, and 19% and 27% of participants, respectively, were diagnosed with skin lesions that required treatment.

Participants in the current study were given no further treatment or advice. Recommendations were made that participants monitor suspicious skin lesions or have them removed. With regard to future screening, 84.4% of participants with at least 1 categorized skin lesion were advised to have a regular follow-up within 1 year, while 15.6% were advised to follow-up within 1 to 2 years. Therefore, a period of 2 years before the next checkup, the period between screenings offered by statutory health insurance providers in Germany,12 was considered too long for the majority of participants, according to the dermatologists involved with our study.

Conclusion

The high rate of suspicious skin lesions diagnosed demonstrated the effectiveness of skin cancer screenings organized in the workplace, which should be recommended for all employees, not only those who are at high risk for developing skin cancer due to the nature of their work, such as those who work outdoors. It should be noted that the study group examined in the current study was a homogeneous group of employees of a technical company only and is therefore relatively selective. Nevertheless, despite the comparatively selective and young participant group, these examinations provide evidence of the importance of skin cancer screening programs for a wider population.

Acknowledgments

The authors thank Heidi Seybold, MD; Petra Wörl, MD; Sybille Thoma-Uszynski, MD; and Jens Bussmann, MD (all from Erlangen, Germany), for their support and active assistance in the practical implementation of this study.

The incidence of skin cancer, along with its effects on patients and the economy, has continued to increase and therefore requires particular attention from dermatologists. UV light has been shown to be of etiopathologic importance in the development of various types of skin cancer.1-3 Studies have shown that there is a direct correlation between the incidence of skin cancer and average annual amounts of UV radiation exposure.3 Accordingly, in 2009 the International Agency for Research on Cancer classified UV light as carcinogenic to humans.4 Therefore, the general public must be made aware of the danger of exposure to UV radiation.

In Australia, government initiatives to educate the population on causes of skin cancer development and its relationship to UV radiation have already caused the public to change their way of thinking and to deal with sunlight in a conscious and responsible manner.5 A large proportion of the Australian population with light skin is at a particularly high risk for developing skin cancer due to intense exposure to UV radiation. Numerous campaigns in Germany and other countries have attempted to sensitize the public to this issue by emphasizing a reduction in UV exposure (primary prevention) or highlighting the importance of early diagnosis (secondary prevention).6,7

For a good prognosis, it is crucial that skin cancer, particularly melanoma, is discovered at an early or precancerous stage.8 For this reason, self-examination of the skin and skin cancer screening are important factors that can contribute to ensuring early and curative treatment.9-11 Since July 1, 2008, skin cancer screenings have been included in the preventative health care program by statutory health insurance providers in Germany. As part of this program, the cost of screening once every 2 years for individuals 35 years and older is covered by statutory health insurance.12 Several studies have shown a decline in the melanoma mortality rate since the introduction of skin cancer screening programs in Germany.11,13,14

Employee skin cancer screening programs are an important method of examining high numbers of individuals quickly and effectively. These programs have been carried out in Germany and other countries.15,16 Studies have shown that skin cancer screening carried out selectively on defined groups can be an effective form of secondary prevention, particularly for those who work outdoors.17

An employee skin cancer screening program was carried out as part of this study. The findings are interpreted and discussed in relation to other employee screening programs that have been reported as well as those introduced by statutory health insurance providers in Germany. The aim of this study was to determine the importance and effectiveness of employee skin cancer screening programs and the role they play in secondary prevention of skin cancer.

Methods

Study Population

Employees of a technical company in Bavaria, Germany, were offered a skin cancer screening program by the employer’s occupational health service and health insurance provider in collaboration with the Department of Dermatology at the University Hospital Erlangen (Erlangen, Germany). Skin examinations were performed exclusively by 5 trained dermatologists. Only direct employees of the company at 3 of its locations in the Erlangen area were eligible to participate. The total number of employees varied by location (1072–5126 employees). The majority of employees had a university education or had completed technical training. Family members and other individuals who were not members of the company were excluded. There were no further inclusion or exclusion criteria. Over a period of 13 days, 783 of 7823 total employees (10.0%) were examined and included in the study. The study was approved by the Responsible Ethics Commission of the Faculty of Medicine at Friedrich-Alexander-University Erlangen-Nürnberg, Germany.

 

 

Study Design

Employees signed a consent form for participation in the study and completed a standardized questionnaire. The questionnaire was based on surveys used in a prior study18 and collected information on current and prior skin lesions, prior dermatological screening, personal and family history of skin tumors, frequency of UV exposure, and type of UV protection used. For the question on measures taken for protection from UV radiation, possible answers included with sunscreen cream, with suitable sun-protective clothing, and by staying in the shade, or no measures were taken. In contrast to the other questions, multiple answers were accepted for this question. Answering no automatically excluded other possible answers. Participants also were asked to assess their own Fitzpatrick skin type19; the questionnaire included explanations of each skin type (I–IV).

The participants were then called in for examination by the dermatologist at 15-minute intervals. All clothing was removed and the skin was examined. Dermatoscopes were used for closer examination of suspicious skin lesions. The clinical results of the examinations were recorded on a standardized form.

An estimation of the number of melanocytic nevi—≤20, 21–49, or ≥50—was recorded for each patient. Suspicious skin lesions were assigned to one of the following categories: nevus requiring future checkup (Nc), nevus requiring excision (Ne), suspected malignant melanoma (MM), suspected squamous cell carcinoma, suspected basal cell carcinoma (BCC), suspected other skin tumor, and precancerous lesion. Fitzpatrick skin type also was assessed for all participants and recorded by the dermatologist carrying out the examination. Each participant was assigned to a risk group—low, moderate, or high risk—based on their individual risk for developing a skin tumor. Factors that were considered when determining participants’ risk for developing skin cancer included Fitzpatrick skin type, number of melanocytic nevi, personal and family history, leisure activities, UV protection used, and current clinical diagnosis of skin lesions.

After the skin examination, participants were informed of recommended treatment but were not given any additional dermatologic advice. Participants could arrange an appointment at the Department of Dermatology, University Hospital Erlangen, for the excision and histological analysis of the skin lesions. All recorded data were collected in a computerized spreadsheet program. When evaluating the questionnaires, questions that were not answered or were answered incorrectly (participant chose more than 1 answer) were ignored.

Statistical Analysis

Statistical analysis was carried out using SPSS software version 16.0. The majority of the data were nominal or ordinal. Metric data were checked for normal distribution using the Shapiro-Wilk test before carrying out parametric tests. Statistical tests were carried out using the χ2 test and the t test for independent samples. Non-nominal distributed data were checked using the Mann-Whitney U test. P<.05 was considered statistically significant in the exploratory data analysis.

Results

Of 783 employees included in the study, 288 (36.8%) were female and 495 (63.2%) were male (Table 1). In comparison with the total workforce, a significantly higher proportion of women than men took part in the cross-sectional study (P<.01). The average age (SD) was 42.3 (9.5) years (range, 18–64 years). Female participants (average age [SD], 39.8 [10.2] years) were significantly younger than male participants (average age [SD], 43.8 [8.8] years; P<.01). Forty-one percent of participants had a prior skin cancer screening. One percent of participants had a personal history of skin cancer, with 1 participant reporting a history of MM; 6.5% had a family history of skin cancer, of which 39.2% had a family history of MM.

The results of the clinical examinations showed that 43.8% of participants had 20 or fewer melanocytic nevi, 43.4% had 21 to 49 melanocytic nevi, and 12.8% had 50 or more melanocytic nevi. Significantly more women than men had 20 or fewer melanocytic nevi (P<.05).

Approximately 92% of participants assessed themselves as having Fitzpatrick skin types II (35.2%) or III (56.7%), while only approximately 3.6% and 4.5% assessed themselves as having skin types I and IV, respectively. The results of the Fitzpatrick skin type assessments made by dermatologists were similar: 96.9% of participants were assessed as having Fitzpatrick skin types II (43.0%) and III (53.8%); approximately 1.9% and 1.3% were assessed as having Fitzpatrick skin types I and IV, respectively. Results showed that 80.2% of all participants assessed their skin type in the same way as the dermatologist; 13.5% assessed their skin type as darker and 6.3% (49/783) assessed it as lighter. A quantitative analysis of Fitzpatrick skin type and sex showed that significantly more male participants than female participants assessed their Fitzpatrick skin type darker than their actual skin type (P<.01).

Overall, 47.6% of participants reported having had sunburn rarely in the past, while 36.9% and 14.0% had experienced sunburn once per year and several times per year, respectively. Approximately 1.4% of participants reported never having a sunburn. More of the male participants made use of comprehensive sun protection using all methods listed (34.5%; P<.05) or a combination of sunscreen and sun-protective clothing (14.9%; P<.01) than the female participants who relied more frequently on sunscreen alone (29.5%; P<.01) or a combination of sunscreen and staying in the shade (29.5%; P<.01)

In general it was clear that sunscreen, either alone or in combination with other sun-protection methods, was used most frequently (88.0%); 58.0% protected themselves by staying in the shade, while 48.0% used suitable sun-protective clothing. Only 3.6% of participants did not protect themselves using any of the suggested methods.

A total of 661 categorized skin lesions were found in 377 participants. Of these lesions, 491 were Nc and 121 were Ne. Twenty-four of the skin lesions were suspected precancerous lesions, 13 were suspected BCC, 2 were suspected MM, and 10 were suspected other skin tumor (Table 2). Overall, male participants who were diagnosed with at least 1 skin lesion (average age, 44.0 years) were significantly older than the women (average age, 39.3 years)(P<.01). Similar findings were observed in participants with at least 1 Nc (men, 43.3 years; women, 38.7 years; P<.01) and at least 1 Ne (men, 44.2 years; women, 38.0 years; P<.05). With regard to the individual risk for developing skin cancer, 32.6% of participants were considered to be at low risk, 64.9% were at moderate risk, and 2.6% were at high risk.

Approximately 61.5% of 377 participants who were diagnosed with at least 1 categorized skin lesion were advised to have a specific skin lesion checked by a dermatologist or to have a full examination for skin cancer once every 12 months. Furthermore, 22.5% were advised to follow-up biannually and 11.7% were advised to follow-up once every 2 years. Of the remaining participants who were advised to have follow-ups, 0.3% were advised to have a skin examination once every 3 months after having had MM, and 4.0% were advised to have follow-up once every 18 months. Overall, follow-up was recommended within 1 year in 84.4% of cases and within 1 to 2 years in 15.6% (Table 3).

Subsequent histological analysis of the excised tissue resulted in a diagnosis of only 21 clinically significant skin conditions. One case of Bowen disease and 1 case of BCC was confirmed. Histological analysis identified the remaining 19 excised skin lesions, which included the 2 suspected MMs, as dysplastic nevi.

 

 

Comment

The aim of this cross-sectional study was to examine the importance and effectiveness of employee skin cancer screening programs. In comparison with the total workforce, significantly more women took part than men. Female participants were significantly younger than male participants, which mirrors the findings of prior studies showing that screening programs reach women more frequently than men and that women who participate in screenings are also younger on average in comparison to men.7-13 Men and older individuals usually are underrepresented.7,13 The average age of participants in our study was 42.3 years, which is lower than in the SCREEN (Skin Cancer Research to Provide Evidence for Effectiveness of Screening in Northern Germany) study (average age, 49.7 years).13 The average age in our study also is likely to be lower than patients who undergo skin cancer screenings offered by statutory health insurance providers in Germany, which has a minimum age restriction of 35 years; however, it is comparable to the average age of participants in other employee screening programs and therefore represents the average age of individuals employed in Germany.15,16

The employee skin cancer screening program in this study generated a high level of interest, indicated by the fact that all available appointments had been booked just 36 hours after the screening was announced. Furthermore, there was a waiting list of approximately 300 employees who were not able to undergo a skin examination. For logistical reasons, the number of participants was limited to 10% of the workforce. The high level of interest is an indication of increased awareness of the importance of recognizing skin tumors early and the associated need for information as well as the need to undergo screening for skin cancer as a precaution. This observation also can be made with regard to the skin cancer screening introduced by statutory health insurance providers in Germany. Studies published by Augustin et al20 and Kornek et al21,22 confirm that skin cancer screenings have gained wide acceptance in Germany because they were introduced by statutory health insurance providers in 2008. The number of skin cancer screenings carried out by dermatologists in Germany also is increasing.20-22 Although approximately 19% of those eligible to participate took part in the SCREEN pilot project,13 approximately 31% of individuals who were eligible to participate took part in skin cancer screenings offered by statutory health insurance providers in Germany in 2012, and the percentage is rising.23 Two important factors affecting the high level of interest in the employee screening program used in our study were undoubtedly the advantages of the examination taking place during working hours and being held on the occupational health services’ premises in the workplace, which helped participants avoid the cost of travel and wait times associated with visiting a medical practice.

Of 783 participants included in this study, 377 displayed at least 1 categorized skin lesion; the majority were suspicious melanocytic nevi. This high incidence rate suggested that regular skin cancer screenings are useful, as it has been shown that there is a correlation between higher numbers of melanocytic nevi and increased risk for developing melanoma.24

In a study by Winkler et al,25 a skin cancer screening of 1658 bank and insurance employees found that 33.8% of those examined displayed at least 1 atypical melanocytic nevus and 27.2% displayed more than 50 melanocytic nevi (compared to 12.8% with ≥50 melanocytic nevi in the current study). The risk for developing skin cancer was classified as intermediate or high in 54.5% (compared to 67.5% at moderate or high risk in the current study).25 Therefore, the rate of suspicious skin lesions was lower in the population of the study by Winkler et al25 in comparison to the population of the current study. As the overall number of melanocytic nevi and the individual risk for skin cancer, however, was underestimated by the majority of the bank and insurance employees,25 employee skin cancer screening programs can be used as a potentially effective tool to make employees aware of the issue and sensitizing them to it. Employee screening in addition to a final diagnosis can contribute to ensuring suitable treatment is started. For example, in the large-scale employee screening published by Schaefer et al15 and Augustin et al,16 48,665 and 90,880 employees, respectively, were screened for inflammatory and noninflammatory skin diseases, and 19% and 27% of participants, respectively, were diagnosed with skin lesions that required treatment.

Participants in the current study were given no further treatment or advice. Recommendations were made that participants monitor suspicious skin lesions or have them removed. With regard to future screening, 84.4% of participants with at least 1 categorized skin lesion were advised to have a regular follow-up within 1 year, while 15.6% were advised to follow-up within 1 to 2 years. Therefore, a period of 2 years before the next checkup, the period between screenings offered by statutory health insurance providers in Germany,12 was considered too long for the majority of participants, according to the dermatologists involved with our study.

Conclusion

The high rate of suspicious skin lesions diagnosed demonstrated the effectiveness of skin cancer screenings organized in the workplace, which should be recommended for all employees, not only those who are at high risk for developing skin cancer due to the nature of their work, such as those who work outdoors. It should be noted that the study group examined in the current study was a homogeneous group of employees of a technical company only and is therefore relatively selective. Nevertheless, despite the comparatively selective and young participant group, these examinations provide evidence of the importance of skin cancer screening programs for a wider population.

Acknowledgments

The authors thank Heidi Seybold, MD; Petra Wörl, MD; Sybille Thoma-Uszynski, MD; and Jens Bussmann, MD (all from Erlangen, Germany), for their support and active assistance in the practical implementation of this study.

References
  1. Boniol M, Autier P, Boyle P, et al. Cutaneous melanoma attributable to sunbed use: systematic review and meta-analysis. BMJ. 2012;345:e4757.
  2. Gilchrest BA, Eller MS, Geller AC, et al. The pathogenesis of melanoma induced by ultraviolet radiation. N Engl J Med. 1999;340:1341-1348.
  3. Rigel DS. Cutaneous ultraviolet exposure and its relationship to the development of skin cancer. J Am Acad Dermatol. 2008;58:129-132.
  4. El Ghissassi F, Baan R, Straif K, et al; WHO International Agency for Research on Cancer Monograph Working Group. A review of human carcinogens—part D: radiation. Lancet Oncol. 2009;10:751-752.
  5. MacLennan R, Green AC, McLeod GR, et al. Increasing incidence of cutaneous melanoma in Queensland, Australia. J Natl Cancer Inst. 1992;84:1427-1432.
  6. Heinzerling LM, Dummer R, Panizzon RG, et al. Prevention campaign against skin cancer. Dermatology. 2002;205:229-233.
  7. Stratigos A, Nikolaou V, Kedicoglou S, et al. Melanoma/skin cancer screening in a Mediterranean country: results of the Euromelanoma Screening Day Campaign in Greece. J Eur Acad Dermatol Venereol. 2007;21:56-62.
  8. Garbe C, Hauschild A, Volkenandt M, et al. Evidence and interdisciplinary consense-based German guidelines: diagnosis and surveillance of melanoma. Melanoma Res. 2007;17:393-399.
  9. Choudhury K, Volkmer B, Greinert R, et al. Effectiveness of skin cancer screening programmes. Br J Dermatol. 2012;167:94-98.
  10. Eisemann N, Waldmann A, Geller AC, et al. Non-melanoma skin cancer incidence and impact of skin cancer screening on incidence. J Invest Dermatol. 2014;134:43-50.
  11. Katalinic A, Waldmann A, Weinstock MA, et al. Does skin cancer screening save lives? an observational study comparing trends in melanoma mortality in regions with and without screening. Cancer. 2012;118:5395-5402.
  12. Bekanntmachung (1430 A) eines Beschlusses des Gemeinsamen Bundeausschusses über eine Änderung der Krebsfrüherkennungs-Richtlinien: Hautkrebs-Screening [press release]. Berlin, Germany: Bundesministerium für Gesundheit (Federal Ministry of Health, Germany); vom 15. November 2007.
  13. Breitbart EW, Waldmann A, Nolte S, et al. Systematic skin cancer screening in Northern Germany. J Am Acad Dermatol. 2012;66:201-211.
  14. Waldmann A, Nolte S, Weinstock MA, et al. Skin cancer screening participation and impact on melanoma incidence in Germany—an observational study on incidence trends in regions with and without population-based screening. Br J Cancer. 2012;106:970-974.
  15. Schaefer I, Rustenbach SJ, Zimmer L, et al. Prevalence of skin diseases in a cohort of 48,665 employees in Germany. Dermatology. 2008;217:169-172.
  16. Augustin M, Herberger K, Hintzen S, et al. Prevalence of skin lesions and need for treatment in a cohort of 90880 workers. Br J Dermatol. 2011;165:865-873.
  17. LeBlanc WG, Vidal L, Kirsner RS, et al. Reported skin cancer screening of US adult workers. J Am Acad Dermatol. 2008;59:55-63.
  18. Harbauer A, Binder M, Pehamberger H, et al. Validity of an unsupervised self-administered questionnaire for self-assessment of melanoma risk. Melanoma Res. 2003;13:537-542.
  19. Fitzpatrick TB. The validity and practicality of sun-reactive skin types I through VI. Arch Dermatol. 1988;124:869-871.
  20. Augustin M, Stadler R, Reusch M, et al. Skin cancer screening in Germany—perception by the public. J Dtsch Dermatol Ges. 2012;10:42-49.
  21. Kornek T, Augustin M. Skin cancer prevention. J Dtsch Dermatol Ges. 2013;11:283-296.
  22. Kornek T, Schäfer I, Reusch M, et al. Routine skin cancer screening in Germany: four years of experience from the dermatologists’ perspective. Dermatology. 2012;225:289-293.
  23. Barmer GEK Arztreport 2014 [press release]. Berlin, Germany: Barmer GEK; February 4, 2014.
  24. Bauer J, Garbe C. Acquired melanocytic nevi as riskfactor for melanoma development. a comprehensive review of epidemiological data. Pigment Cell Res. 2003;16:297-306.
  25. Winkler A, Plugfelder A, Weide B, et al. Screening for skin cancer in bank and insurance employees: risk profile and correlation of self and physician’s assessment. Int J Dermatol. 2015;54:419-423.
References
  1. Boniol M, Autier P, Boyle P, et al. Cutaneous melanoma attributable to sunbed use: systematic review and meta-analysis. BMJ. 2012;345:e4757.
  2. Gilchrest BA, Eller MS, Geller AC, et al. The pathogenesis of melanoma induced by ultraviolet radiation. N Engl J Med. 1999;340:1341-1348.
  3. Rigel DS. Cutaneous ultraviolet exposure and its relationship to the development of skin cancer. J Am Acad Dermatol. 2008;58:129-132.
  4. El Ghissassi F, Baan R, Straif K, et al; WHO International Agency for Research on Cancer Monograph Working Group. A review of human carcinogens—part D: radiation. Lancet Oncol. 2009;10:751-752.
  5. MacLennan R, Green AC, McLeod GR, et al. Increasing incidence of cutaneous melanoma in Queensland, Australia. J Natl Cancer Inst. 1992;84:1427-1432.
  6. Heinzerling LM, Dummer R, Panizzon RG, et al. Prevention campaign against skin cancer. Dermatology. 2002;205:229-233.
  7. Stratigos A, Nikolaou V, Kedicoglou S, et al. Melanoma/skin cancer screening in a Mediterranean country: results of the Euromelanoma Screening Day Campaign in Greece. J Eur Acad Dermatol Venereol. 2007;21:56-62.
  8. Garbe C, Hauschild A, Volkenandt M, et al. Evidence and interdisciplinary consense-based German guidelines: diagnosis and surveillance of melanoma. Melanoma Res. 2007;17:393-399.
  9. Choudhury K, Volkmer B, Greinert R, et al. Effectiveness of skin cancer screening programmes. Br J Dermatol. 2012;167:94-98.
  10. Eisemann N, Waldmann A, Geller AC, et al. Non-melanoma skin cancer incidence and impact of skin cancer screening on incidence. J Invest Dermatol. 2014;134:43-50.
  11. Katalinic A, Waldmann A, Weinstock MA, et al. Does skin cancer screening save lives? an observational study comparing trends in melanoma mortality in regions with and without screening. Cancer. 2012;118:5395-5402.
  12. Bekanntmachung (1430 A) eines Beschlusses des Gemeinsamen Bundeausschusses über eine Änderung der Krebsfrüherkennungs-Richtlinien: Hautkrebs-Screening [press release]. Berlin, Germany: Bundesministerium für Gesundheit (Federal Ministry of Health, Germany); vom 15. November 2007.
  13. Breitbart EW, Waldmann A, Nolte S, et al. Systematic skin cancer screening in Northern Germany. J Am Acad Dermatol. 2012;66:201-211.
  14. Waldmann A, Nolte S, Weinstock MA, et al. Skin cancer screening participation and impact on melanoma incidence in Germany—an observational study on incidence trends in regions with and without population-based screening. Br J Cancer. 2012;106:970-974.
  15. Schaefer I, Rustenbach SJ, Zimmer L, et al. Prevalence of skin diseases in a cohort of 48,665 employees in Germany. Dermatology. 2008;217:169-172.
  16. Augustin M, Herberger K, Hintzen S, et al. Prevalence of skin lesions and need for treatment in a cohort of 90880 workers. Br J Dermatol. 2011;165:865-873.
  17. LeBlanc WG, Vidal L, Kirsner RS, et al. Reported skin cancer screening of US adult workers. J Am Acad Dermatol. 2008;59:55-63.
  18. Harbauer A, Binder M, Pehamberger H, et al. Validity of an unsupervised self-administered questionnaire for self-assessment of melanoma risk. Melanoma Res. 2003;13:537-542.
  19. Fitzpatrick TB. The validity and practicality of sun-reactive skin types I through VI. Arch Dermatol. 1988;124:869-871.
  20. Augustin M, Stadler R, Reusch M, et al. Skin cancer screening in Germany—perception by the public. J Dtsch Dermatol Ges. 2012;10:42-49.
  21. Kornek T, Augustin M. Skin cancer prevention. J Dtsch Dermatol Ges. 2013;11:283-296.
  22. Kornek T, Schäfer I, Reusch M, et al. Routine skin cancer screening in Germany: four years of experience from the dermatologists’ perspective. Dermatology. 2012;225:289-293.
  23. Barmer GEK Arztreport 2014 [press release]. Berlin, Germany: Barmer GEK; February 4, 2014.
  24. Bauer J, Garbe C. Acquired melanocytic nevi as riskfactor for melanoma development. a comprehensive review of epidemiological data. Pigment Cell Res. 2003;16:297-306.
  25. Winkler A, Plugfelder A, Weide B, et al. Screening for skin cancer in bank and insurance employees: risk profile and correlation of self and physician’s assessment. Int J Dermatol. 2015;54:419-423.
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Practice Points

  • Employee skin cancer screening programs are an important method of examining high numbers of individuals quickly and efficiently and should be used as an important tool for secondary skin cancer prevention.
  • The high rate of suspicious skin lesions diagnosed in this study demonstrates the effectiveness of skin cancer screenings organized in the workplace and provides evidence of the importance of skin cancer screening programs for a wider population.
  • Employee skin cancer screening programs should be recommended for all employees, not only those who are at high risk for developing skin cancer due to the nature of their work, such as those who work outdoors.
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Subungual Onycholemmal Cyst of the Toenail Mimicking Subungual Melanoma

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Subungual Onycholemmal Cyst of the Toenail Mimicking Subungual Melanoma

Case Report

A 23-year-old woman presented with a horizontal split along the midline of the right great toenail associated with some tenderness of 2 to 3 months’ duration. Approximately 5 years prior, she noticed a bluish-colored area under the nail that had been steadily increasing in size. She denied a history of trauma, drainage, or bleeding. There was no history of other nail abnormalities. Her medications and personal, family, and social history were noncontributory.

Physical examination of the right great toenail revealed a horizontal split of the nail plate with a bluish hue visible under the nail plate (Figure 1A). The remaining toenails and fingernails were normal. A punch biopsy of the nail bed was performed with a presumptive clinical diagnosis of subungual melanoma versus melanocytic nevus versus cyst (Figure 1B). Nail plate avulsion revealed a blackened nail bed dotted with areas of bluish color and a red friable nodule present focally. Upon further inspection, extension was apparent into the distal matrix.

Figure 1. Subungual pressure-induced onycholysis overlying bluish discoloration of the lateral third of the right great toenail. The proximal and lateral nail folds were unaffected (A). A 4-mm punch biopsy site was visible on the nail bed following partial nail avulsion (B).

Histopathologic examination revealed a cystic structure with an epithelial lining mostly reminiscent of an isthmus catagen cyst admixed with the presence of both an intermittent focal granular layer and an eosinophilic cuticle surrounding pink laminated keratin, most consistent with a diagnosis of subungual onycholemmal cyst (SOC)(Figure 2). A reexcision was performed with removal of half of the nail bed, including a portion of the distal matrix extending inferiorly to the bone. Variably sized, epithelium-lined, keratin-filled cystic structures emanated from the nail bed epithelium. There were foci of hemorrhage and granulation tissue secondary to cyst rupture (Figure 3). The defect healed by secondary intention. No clinical evidence of recurrence was seen at 6-month follow-up.

Figure 2. Histopathology revealed a cystic structure with an epithelial lining with an intermittent focal granular layer and eosinophilic cuticle surrounding pink laminated keratin, most consistent with a diagnosis of a subungual onycholemmal cyst (A and B).

Figure 3. The gross specimen after reexcision revealed multiple foci of hemorrhage and brown keratinaceous material (A). Scanning magnification revealed variably sized, epithelium-lined, keratin-filled cystic structures emanating from the nail bed epithelium containing foci of calcification. There was hemorrhage and granulation tissue secondary to cyst rupture (B)(H&E, original magnification ×20).
Comment

Subungual onycholemmal cysts, also known as subungual epidermoid cysts or subungual epidermoid inclusions, are rare and distinctive nail abnormalities occurring in the dermis of the nail bed. We present a case of an SOC in a toenail mimicking subungual malignant melanoma.

Originally described by Samman1 in 1959, SOCs were attributed to trauma to the nail with resultant implantation of the epidermis into the deeper tissue. Lewin2,3 examined 90 postmortem fingernail and nail bed samples and found 8 subungual epidermoid cysts associated with clubbing of the fingernails. He postulated that the early pathogenesis of clubbing involved dermal fibroblast proliferation in the nail bed, leading to sequestration of nail bed epithelium into the dermis with resultant cyst formation. Microscopic subungual cysts also were identified in normal-appearing nails without evidence of trauma, thought to have arisen from the tips of the nail bed rete ridges by a process of bulbous proliferation rather than sequestration. These findings in normal nails suggest that SOCs may represent a more common entity than previously recognized.

 

 

It is imperative to recognize the presence of nail unit tumors early because of the risk for permanent nail plate dystrophy and the possibility of a malignant tumor.4,5 Subungual onycholemmal cysts may present with a wide spectrum of clinical findings including marked subungual hyperkeratosis, onychodystrophy, ridging, nail bed pigmentation, clubbing, thickening, or less often a normal-appearing nail. Based on reported cases, several trends are evident. Although nail dystrophy is most often asymptomatic, pain is not uncommon.5,6 It most commonly involves single digits, predominantly thumbs and great toenails.7,8 This predilection suggests that trauma or other local factors may be involved in its pathogenesis. Of note, trauma to the nail may occur years before the development of the lesions or it may not be recalled at all.

Diagnosis requires a degree of clinical suspicion and a nail bed biopsy with partial or total nail plate avulsion to visualize the pathologic portion of the nail bed. Because surgical intervention may lead to the implantation of epithelium, recurrences after nail biopsy or excision may occur.

In contrast to epidermal inclusion cysts arising in the skin, most SOCs do not have a granular layer.9 Hair and nails represent analogous differentiation products of the ectoderm. The nail matrix is homologous to portions of the hair matrix, while the nail bed epithelium is comparable to the outer root sheath of the hair follicle.7 Subungual onycholemmal cysts originate from the nail bed epithelium, which keratinizes in the absence of a granular layer, similar to the follicular isthmus outer root sheath. Thus, SOCs are comparable to the outer root sheath–derived isthmus-catagen cysts because of their abrupt central keratinization.8

Subungual onycholemmal cysts also must be distinguished from slowly growing malignant tumors of the nail bed epithelium, referred to as onycholemmal carcinomas by Alessi et al.10 This entity characteristically presents in elderly patients as a slowly growing, circumscribed, subungual discoloration that may ulcerate, destroying the nail apparatus and penetrating the phalangeal bone. On histopathology, it is characterized by small cysts filled with eosinophilic keratin devoid of a granular layer and lined by atypical squamous epithelium accompanied by solid nests and strands of atypical keratinocytes within the dermis.11 When a cystic component and clear cells predominate, the designation of malignant proliferating onycholemmal cyst has been applied. Its infiltrative growth pattern with destruction of the underlying bone makes it an important entity to exclude when considering the differential diagnosis of tumors of the nail bed.

Subungual melanomas comprise only 1% to 3% of malignant melanomas and 85% are initially misdiagnosed due to their rarity and nonspecific variable presentation. Aside from clinical evidence of Hutchinson sign in the early stages in almost all cases, accurate diagnosis of subungual melanoma and differentiation from SOCs relies on histopathology. A biopsy is necessary to make the diagnosis, but even microscopic findings may be nonspecific during the early stages.

Conclusion

We report a case of a 23-year-old woman with horizontal ridging and tenderness of the right great toenail associated with pigmentation of 5 years’ duration due to an SOC. The etiology of these subungual cysts, with or without nail abnormalities, still remains unclear. Its predilection for the thumbs and great toenails suggests that trauma or other local factors may be involved in its pathogenesis. Because of the rarity of this entity, there are no guidelines for surgical treatment. Subungual onycholemmal cysts may be an underrecognized and more common entity that must be considered when discussing tumors of the nail unit.

References
  1. Samman PD. The human toe nail. its genesis and blood supply. Br J Dermatol. 1959;71:296-302.
  2. Lewin K. The normal fingernail. Br J Dermatol. 1965;77:421-430.
  3. Lewin K. Subungual epidermoid inclusions. Br J Dermatol. 1969;81:671-675.
  4. Dominguez-Cherit J, Chanussot-Deprez C, Maria-Sarti H, et al. Nail unit tumors: a study of 234 patients in the dermatology department of the “Dr. Manuel Gea González” General Hospital in Mexico City. Dermatol Surg. 2008;34:1363-1371.
  5. Sáez-de-Ocariz MM, Domínguez-Cherit J, García-Corona C. Subungual epidermoid cysts. Int J Dermatol. 2001;40:524-526.
  6. Molly DO, Herbert K. Subungual epidermoid cyst. J Hand Surg Br. 2006;31:345.
  7. Telang GH, Jellinek N. Multiple calcified subungual epidermoid inclusions. J Am Acad Dermatol. 2007;56:336-339.
  8. Fanti PA, Tosti A. Subungual epidermoid inclusions: report of 8 cases. Dermatologica. 1989;178:209-212.
  9. Takiyoshi N, Nakano H, Matsuzaki T, et al. An eclipse in the subungual space: a diagnostic sign for a subungual epidermal cyst? Br J Dermatol. 2009;161:962-963.
  10. Alessi E, Coggi A, Gianotti R, et al. Onycholemmal carcinoma. Am J Dermatopathol. 2004;26:397-402.
  11. Inaoki M, Makino E, Adachi M, et al. Onycholemmal carcinoma. J Cutan Pathol. 2006;33:577-580.
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Drs. Busquets, Campanelli, Sahu, and Lee are from the Department of Dermatology and Cutaneous Biology, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania. Dr. Banala is from Jefferson Medical College, Thomas Jefferson University, Philadelphia.

The authors report no conflict of interest.

Correspondence: Joanna Busquets, MD, Thomas Jefferson University Hospital, Department of Dermatology and Cutaneous Biology, 833 Chestnut St, Ste 740, Philadelphia, PA 19107 ([email protected]).

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Drs. Busquets, Campanelli, Sahu, and Lee are from the Department of Dermatology and Cutaneous Biology, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania. Dr. Banala is from Jefferson Medical College, Thomas Jefferson University, Philadelphia.

The authors report no conflict of interest.

Correspondence: Joanna Busquets, MD, Thomas Jefferson University Hospital, Department of Dermatology and Cutaneous Biology, 833 Chestnut St, Ste 740, Philadelphia, PA 19107 ([email protected]).

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Drs. Busquets, Campanelli, Sahu, and Lee are from the Department of Dermatology and Cutaneous Biology, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania. Dr. Banala is from Jefferson Medical College, Thomas Jefferson University, Philadelphia.

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Correspondence: Joanna Busquets, MD, Thomas Jefferson University Hospital, Department of Dermatology and Cutaneous Biology, 833 Chestnut St, Ste 740, Philadelphia, PA 19107 ([email protected]).

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Case Report

A 23-year-old woman presented with a horizontal split along the midline of the right great toenail associated with some tenderness of 2 to 3 months’ duration. Approximately 5 years prior, she noticed a bluish-colored area under the nail that had been steadily increasing in size. She denied a history of trauma, drainage, or bleeding. There was no history of other nail abnormalities. Her medications and personal, family, and social history were noncontributory.

Physical examination of the right great toenail revealed a horizontal split of the nail plate with a bluish hue visible under the nail plate (Figure 1A). The remaining toenails and fingernails were normal. A punch biopsy of the nail bed was performed with a presumptive clinical diagnosis of subungual melanoma versus melanocytic nevus versus cyst (Figure 1B). Nail plate avulsion revealed a blackened nail bed dotted with areas of bluish color and a red friable nodule present focally. Upon further inspection, extension was apparent into the distal matrix.

Figure 1. Subungual pressure-induced onycholysis overlying bluish discoloration of the lateral third of the right great toenail. The proximal and lateral nail folds were unaffected (A). A 4-mm punch biopsy site was visible on the nail bed following partial nail avulsion (B).

Histopathologic examination revealed a cystic structure with an epithelial lining mostly reminiscent of an isthmus catagen cyst admixed with the presence of both an intermittent focal granular layer and an eosinophilic cuticle surrounding pink laminated keratin, most consistent with a diagnosis of subungual onycholemmal cyst (SOC)(Figure 2). A reexcision was performed with removal of half of the nail bed, including a portion of the distal matrix extending inferiorly to the bone. Variably sized, epithelium-lined, keratin-filled cystic structures emanated from the nail bed epithelium. There were foci of hemorrhage and granulation tissue secondary to cyst rupture (Figure 3). The defect healed by secondary intention. No clinical evidence of recurrence was seen at 6-month follow-up.

Figure 2. Histopathology revealed a cystic structure with an epithelial lining with an intermittent focal granular layer and eosinophilic cuticle surrounding pink laminated keratin, most consistent with a diagnosis of a subungual onycholemmal cyst (A and B).

Figure 3. The gross specimen after reexcision revealed multiple foci of hemorrhage and brown keratinaceous material (A). Scanning magnification revealed variably sized, epithelium-lined, keratin-filled cystic structures emanating from the nail bed epithelium containing foci of calcification. There was hemorrhage and granulation tissue secondary to cyst rupture (B)(H&E, original magnification ×20).
Comment

Subungual onycholemmal cysts, also known as subungual epidermoid cysts or subungual epidermoid inclusions, are rare and distinctive nail abnormalities occurring in the dermis of the nail bed. We present a case of an SOC in a toenail mimicking subungual malignant melanoma.

Originally described by Samman1 in 1959, SOCs were attributed to trauma to the nail with resultant implantation of the epidermis into the deeper tissue. Lewin2,3 examined 90 postmortem fingernail and nail bed samples and found 8 subungual epidermoid cysts associated with clubbing of the fingernails. He postulated that the early pathogenesis of clubbing involved dermal fibroblast proliferation in the nail bed, leading to sequestration of nail bed epithelium into the dermis with resultant cyst formation. Microscopic subungual cysts also were identified in normal-appearing nails without evidence of trauma, thought to have arisen from the tips of the nail bed rete ridges by a process of bulbous proliferation rather than sequestration. These findings in normal nails suggest that SOCs may represent a more common entity than previously recognized.

 

 

It is imperative to recognize the presence of nail unit tumors early because of the risk for permanent nail plate dystrophy and the possibility of a malignant tumor.4,5 Subungual onycholemmal cysts may present with a wide spectrum of clinical findings including marked subungual hyperkeratosis, onychodystrophy, ridging, nail bed pigmentation, clubbing, thickening, or less often a normal-appearing nail. Based on reported cases, several trends are evident. Although nail dystrophy is most often asymptomatic, pain is not uncommon.5,6 It most commonly involves single digits, predominantly thumbs and great toenails.7,8 This predilection suggests that trauma or other local factors may be involved in its pathogenesis. Of note, trauma to the nail may occur years before the development of the lesions or it may not be recalled at all.

Diagnosis requires a degree of clinical suspicion and a nail bed biopsy with partial or total nail plate avulsion to visualize the pathologic portion of the nail bed. Because surgical intervention may lead to the implantation of epithelium, recurrences after nail biopsy or excision may occur.

In contrast to epidermal inclusion cysts arising in the skin, most SOCs do not have a granular layer.9 Hair and nails represent analogous differentiation products of the ectoderm. The nail matrix is homologous to portions of the hair matrix, while the nail bed epithelium is comparable to the outer root sheath of the hair follicle.7 Subungual onycholemmal cysts originate from the nail bed epithelium, which keratinizes in the absence of a granular layer, similar to the follicular isthmus outer root sheath. Thus, SOCs are comparable to the outer root sheath–derived isthmus-catagen cysts because of their abrupt central keratinization.8

Subungual onycholemmal cysts also must be distinguished from slowly growing malignant tumors of the nail bed epithelium, referred to as onycholemmal carcinomas by Alessi et al.10 This entity characteristically presents in elderly patients as a slowly growing, circumscribed, subungual discoloration that may ulcerate, destroying the nail apparatus and penetrating the phalangeal bone. On histopathology, it is characterized by small cysts filled with eosinophilic keratin devoid of a granular layer and lined by atypical squamous epithelium accompanied by solid nests and strands of atypical keratinocytes within the dermis.11 When a cystic component and clear cells predominate, the designation of malignant proliferating onycholemmal cyst has been applied. Its infiltrative growth pattern with destruction of the underlying bone makes it an important entity to exclude when considering the differential diagnosis of tumors of the nail bed.

Subungual melanomas comprise only 1% to 3% of malignant melanomas and 85% are initially misdiagnosed due to their rarity and nonspecific variable presentation. Aside from clinical evidence of Hutchinson sign in the early stages in almost all cases, accurate diagnosis of subungual melanoma and differentiation from SOCs relies on histopathology. A biopsy is necessary to make the diagnosis, but even microscopic findings may be nonspecific during the early stages.

Conclusion

We report a case of a 23-year-old woman with horizontal ridging and tenderness of the right great toenail associated with pigmentation of 5 years’ duration due to an SOC. The etiology of these subungual cysts, with or without nail abnormalities, still remains unclear. Its predilection for the thumbs and great toenails suggests that trauma or other local factors may be involved in its pathogenesis. Because of the rarity of this entity, there are no guidelines for surgical treatment. Subungual onycholemmal cysts may be an underrecognized and more common entity that must be considered when discussing tumors of the nail unit.

Case Report

A 23-year-old woman presented with a horizontal split along the midline of the right great toenail associated with some tenderness of 2 to 3 months’ duration. Approximately 5 years prior, she noticed a bluish-colored area under the nail that had been steadily increasing in size. She denied a history of trauma, drainage, or bleeding. There was no history of other nail abnormalities. Her medications and personal, family, and social history were noncontributory.

Physical examination of the right great toenail revealed a horizontal split of the nail plate with a bluish hue visible under the nail plate (Figure 1A). The remaining toenails and fingernails were normal. A punch biopsy of the nail bed was performed with a presumptive clinical diagnosis of subungual melanoma versus melanocytic nevus versus cyst (Figure 1B). Nail plate avulsion revealed a blackened nail bed dotted with areas of bluish color and a red friable nodule present focally. Upon further inspection, extension was apparent into the distal matrix.

Figure 1. Subungual pressure-induced onycholysis overlying bluish discoloration of the lateral third of the right great toenail. The proximal and lateral nail folds were unaffected (A). A 4-mm punch biopsy site was visible on the nail bed following partial nail avulsion (B).

Histopathologic examination revealed a cystic structure with an epithelial lining mostly reminiscent of an isthmus catagen cyst admixed with the presence of both an intermittent focal granular layer and an eosinophilic cuticle surrounding pink laminated keratin, most consistent with a diagnosis of subungual onycholemmal cyst (SOC)(Figure 2). A reexcision was performed with removal of half of the nail bed, including a portion of the distal matrix extending inferiorly to the bone. Variably sized, epithelium-lined, keratin-filled cystic structures emanated from the nail bed epithelium. There were foci of hemorrhage and granulation tissue secondary to cyst rupture (Figure 3). The defect healed by secondary intention. No clinical evidence of recurrence was seen at 6-month follow-up.

Figure 2. Histopathology revealed a cystic structure with an epithelial lining with an intermittent focal granular layer and eosinophilic cuticle surrounding pink laminated keratin, most consistent with a diagnosis of a subungual onycholemmal cyst (A and B).

Figure 3. The gross specimen after reexcision revealed multiple foci of hemorrhage and brown keratinaceous material (A). Scanning magnification revealed variably sized, epithelium-lined, keratin-filled cystic structures emanating from the nail bed epithelium containing foci of calcification. There was hemorrhage and granulation tissue secondary to cyst rupture (B)(H&E, original magnification ×20).
Comment

Subungual onycholemmal cysts, also known as subungual epidermoid cysts or subungual epidermoid inclusions, are rare and distinctive nail abnormalities occurring in the dermis of the nail bed. We present a case of an SOC in a toenail mimicking subungual malignant melanoma.

Originally described by Samman1 in 1959, SOCs were attributed to trauma to the nail with resultant implantation of the epidermis into the deeper tissue. Lewin2,3 examined 90 postmortem fingernail and nail bed samples and found 8 subungual epidermoid cysts associated with clubbing of the fingernails. He postulated that the early pathogenesis of clubbing involved dermal fibroblast proliferation in the nail bed, leading to sequestration of nail bed epithelium into the dermis with resultant cyst formation. Microscopic subungual cysts also were identified in normal-appearing nails without evidence of trauma, thought to have arisen from the tips of the nail bed rete ridges by a process of bulbous proliferation rather than sequestration. These findings in normal nails suggest that SOCs may represent a more common entity than previously recognized.

 

 

It is imperative to recognize the presence of nail unit tumors early because of the risk for permanent nail plate dystrophy and the possibility of a malignant tumor.4,5 Subungual onycholemmal cysts may present with a wide spectrum of clinical findings including marked subungual hyperkeratosis, onychodystrophy, ridging, nail bed pigmentation, clubbing, thickening, or less often a normal-appearing nail. Based on reported cases, several trends are evident. Although nail dystrophy is most often asymptomatic, pain is not uncommon.5,6 It most commonly involves single digits, predominantly thumbs and great toenails.7,8 This predilection suggests that trauma or other local factors may be involved in its pathogenesis. Of note, trauma to the nail may occur years before the development of the lesions or it may not be recalled at all.

Diagnosis requires a degree of clinical suspicion and a nail bed biopsy with partial or total nail plate avulsion to visualize the pathologic portion of the nail bed. Because surgical intervention may lead to the implantation of epithelium, recurrences after nail biopsy or excision may occur.

In contrast to epidermal inclusion cysts arising in the skin, most SOCs do not have a granular layer.9 Hair and nails represent analogous differentiation products of the ectoderm. The nail matrix is homologous to portions of the hair matrix, while the nail bed epithelium is comparable to the outer root sheath of the hair follicle.7 Subungual onycholemmal cysts originate from the nail bed epithelium, which keratinizes in the absence of a granular layer, similar to the follicular isthmus outer root sheath. Thus, SOCs are comparable to the outer root sheath–derived isthmus-catagen cysts because of their abrupt central keratinization.8

Subungual onycholemmal cysts also must be distinguished from slowly growing malignant tumors of the nail bed epithelium, referred to as onycholemmal carcinomas by Alessi et al.10 This entity characteristically presents in elderly patients as a slowly growing, circumscribed, subungual discoloration that may ulcerate, destroying the nail apparatus and penetrating the phalangeal bone. On histopathology, it is characterized by small cysts filled with eosinophilic keratin devoid of a granular layer and lined by atypical squamous epithelium accompanied by solid nests and strands of atypical keratinocytes within the dermis.11 When a cystic component and clear cells predominate, the designation of malignant proliferating onycholemmal cyst has been applied. Its infiltrative growth pattern with destruction of the underlying bone makes it an important entity to exclude when considering the differential diagnosis of tumors of the nail bed.

Subungual melanomas comprise only 1% to 3% of malignant melanomas and 85% are initially misdiagnosed due to their rarity and nonspecific variable presentation. Aside from clinical evidence of Hutchinson sign in the early stages in almost all cases, accurate diagnosis of subungual melanoma and differentiation from SOCs relies on histopathology. A biopsy is necessary to make the diagnosis, but even microscopic findings may be nonspecific during the early stages.

Conclusion

We report a case of a 23-year-old woman with horizontal ridging and tenderness of the right great toenail associated with pigmentation of 5 years’ duration due to an SOC. The etiology of these subungual cysts, with or without nail abnormalities, still remains unclear. Its predilection for the thumbs and great toenails suggests that trauma or other local factors may be involved in its pathogenesis. Because of the rarity of this entity, there are no guidelines for surgical treatment. Subungual onycholemmal cysts may be an underrecognized and more common entity that must be considered when discussing tumors of the nail unit.

References
  1. Samman PD. The human toe nail. its genesis and blood supply. Br J Dermatol. 1959;71:296-302.
  2. Lewin K. The normal fingernail. Br J Dermatol. 1965;77:421-430.
  3. Lewin K. Subungual epidermoid inclusions. Br J Dermatol. 1969;81:671-675.
  4. Dominguez-Cherit J, Chanussot-Deprez C, Maria-Sarti H, et al. Nail unit tumors: a study of 234 patients in the dermatology department of the “Dr. Manuel Gea González” General Hospital in Mexico City. Dermatol Surg. 2008;34:1363-1371.
  5. Sáez-de-Ocariz MM, Domínguez-Cherit J, García-Corona C. Subungual epidermoid cysts. Int J Dermatol. 2001;40:524-526.
  6. Molly DO, Herbert K. Subungual epidermoid cyst. J Hand Surg Br. 2006;31:345.
  7. Telang GH, Jellinek N. Multiple calcified subungual epidermoid inclusions. J Am Acad Dermatol. 2007;56:336-339.
  8. Fanti PA, Tosti A. Subungual epidermoid inclusions: report of 8 cases. Dermatologica. 1989;178:209-212.
  9. Takiyoshi N, Nakano H, Matsuzaki T, et al. An eclipse in the subungual space: a diagnostic sign for a subungual epidermal cyst? Br J Dermatol. 2009;161:962-963.
  10. Alessi E, Coggi A, Gianotti R, et al. Onycholemmal carcinoma. Am J Dermatopathol. 2004;26:397-402.
  11. Inaoki M, Makino E, Adachi M, et al. Onycholemmal carcinoma. J Cutan Pathol. 2006;33:577-580.
References
  1. Samman PD. The human toe nail. its genesis and blood supply. Br J Dermatol. 1959;71:296-302.
  2. Lewin K. The normal fingernail. Br J Dermatol. 1965;77:421-430.
  3. Lewin K. Subungual epidermoid inclusions. Br J Dermatol. 1969;81:671-675.
  4. Dominguez-Cherit J, Chanussot-Deprez C, Maria-Sarti H, et al. Nail unit tumors: a study of 234 patients in the dermatology department of the “Dr. Manuel Gea González” General Hospital in Mexico City. Dermatol Surg. 2008;34:1363-1371.
  5. Sáez-de-Ocariz MM, Domínguez-Cherit J, García-Corona C. Subungual epidermoid cysts. Int J Dermatol. 2001;40:524-526.
  6. Molly DO, Herbert K. Subungual epidermoid cyst. J Hand Surg Br. 2006;31:345.
  7. Telang GH, Jellinek N. Multiple calcified subungual epidermoid inclusions. J Am Acad Dermatol. 2007;56:336-339.
  8. Fanti PA, Tosti A. Subungual epidermoid inclusions: report of 8 cases. Dermatologica. 1989;178:209-212.
  9. Takiyoshi N, Nakano H, Matsuzaki T, et al. An eclipse in the subungual space: a diagnostic sign for a subungual epidermal cyst? Br J Dermatol. 2009;161:962-963.
  10. Alessi E, Coggi A, Gianotti R, et al. Onycholemmal carcinoma. Am J Dermatopathol. 2004;26:397-402.
  11. Inaoki M, Makino E, Adachi M, et al. Onycholemmal carcinoma. J Cutan Pathol. 2006;33:577-580.
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Subungual Onycholemmal Cyst of the Toenail Mimicking Subungual Melanoma
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  • Trauma to the nail may occur years before the development of subungual onycholemmal cysts or it may not be recalled at all.
  • Diagnosis requires a degree of clinical suspicion and a nail bed biopsy.
  • Subungual onycholemmal cysts must be distinguished from slowly growing malignant tumors of the nail bed epithelium.
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Skip SNL biopsy for desmoplastic melanoma

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SEATTLE – Sentinel lymph node biopsy in patients with head or neck desmoplastic melanoma is positive only 6% of the time, and it doesn’t change the risk of recurrence.

Although sentinel lymph node biopsy (SLNB) is routine in more common forms of cutaneous melanoma, findings from a retrospective case-control study suggest that it’s “not really necessary” for desmoplastic melanoma (DM) of the head or neck, said lead investigator Dylan Roden, MD, of the department of otolaryngology, New York University. General surgeons have pretty much come to that conclusion for DM elsewhere on the body, but it hasn’t been shown before for neck and head lesions, he said.

Dr. Dylan Roden

DM, an invasive form of melanoma in which malignant cells are surrounded by fibrous tissue, accounts for maybe 2% of cutaneous melanomas, with half or so presenting on the head or neck. The reason SLNB is of less use than with other melanomas is that DM “doesn’t often spread through the lymphatics. It’s not that patients won’t ever have metastases, but maybe it will be through the blood. Removing a lymph node won’t necessarily” detect it, Dr. Roden said at the International Conference on Head and Neck Cancer, held by the American Head and Neck Society.

Forgoing SLNB has the added benefit of shaving an hour and a half or more off surgery, which is important since DM patients tend to be older, he added.

The NYU team matched 32 of their cases with 60 controls with more common superficial spreading or nodular melanoma of the head and neck, based on age, gender, ulceration status, and tumor stage. Mean tumor thickness in both groups was more than 4 mm.

SLNB was performed in 16 DM patients (50%) and 36 control patients (60%); it was positive in one DM patient (6.3%) versus 8 of 28 controls with reported results (28.6%).

Eleven DM patients (34%) had a recurrence, which was less frequent then in controls, where 33 patients (55%) had a recurrence (P = .05). “SNLB did not change the risk of overall or regional recurrence” in DM, Dr. Roden said.

Recurrence was more than twice as likely in control patients (odds ratio, 2.33; P = .06). Meanwhile, recurrence in DM was linked to perineural invasion (P = .02), but not ulceration status (P = .12) or mitoses (P = .40).

DM patients also had better 5-year overall survival (79% versus 62%) and disease-free survival (70% versus 42%; P for both = .06). In general, DM “has a more favorable prognosis,” Dr. Roden said.

Cases and controls were in their mid-60s, on average, and most were men. Ulceration was present in about a quarter of patients. Mitosis was more common in superficial spreading and nodular patients (92% versus 53%; P less than .001), while perineural invasion was more common in DM (40% versus 7%; P less than.001).

Although outcomes were more favorable for DM, previous studies have found a higher rate of sentinel lymph node metastases – above 20% – for DM lesions with mixed, rather than pure, pathology. The 6.3% positive SLNB rate at NYU is more in line with what’s been reported before for pure lesions. The team plans to look into the matter.

There was no outside funding for the work, and Dr. Roden had no disclosures.

[email protected]

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SEATTLE – Sentinel lymph node biopsy in patients with head or neck desmoplastic melanoma is positive only 6% of the time, and it doesn’t change the risk of recurrence.

Although sentinel lymph node biopsy (SLNB) is routine in more common forms of cutaneous melanoma, findings from a retrospective case-control study suggest that it’s “not really necessary” for desmoplastic melanoma (DM) of the head or neck, said lead investigator Dylan Roden, MD, of the department of otolaryngology, New York University. General surgeons have pretty much come to that conclusion for DM elsewhere on the body, but it hasn’t been shown before for neck and head lesions, he said.

Dr. Dylan Roden

DM, an invasive form of melanoma in which malignant cells are surrounded by fibrous tissue, accounts for maybe 2% of cutaneous melanomas, with half or so presenting on the head or neck. The reason SLNB is of less use than with other melanomas is that DM “doesn’t often spread through the lymphatics. It’s not that patients won’t ever have metastases, but maybe it will be through the blood. Removing a lymph node won’t necessarily” detect it, Dr. Roden said at the International Conference on Head and Neck Cancer, held by the American Head and Neck Society.

Forgoing SLNB has the added benefit of shaving an hour and a half or more off surgery, which is important since DM patients tend to be older, he added.

The NYU team matched 32 of their cases with 60 controls with more common superficial spreading or nodular melanoma of the head and neck, based on age, gender, ulceration status, and tumor stage. Mean tumor thickness in both groups was more than 4 mm.

SLNB was performed in 16 DM patients (50%) and 36 control patients (60%); it was positive in one DM patient (6.3%) versus 8 of 28 controls with reported results (28.6%).

Eleven DM patients (34%) had a recurrence, which was less frequent then in controls, where 33 patients (55%) had a recurrence (P = .05). “SNLB did not change the risk of overall or regional recurrence” in DM, Dr. Roden said.

Recurrence was more than twice as likely in control patients (odds ratio, 2.33; P = .06). Meanwhile, recurrence in DM was linked to perineural invasion (P = .02), but not ulceration status (P = .12) or mitoses (P = .40).

DM patients also had better 5-year overall survival (79% versus 62%) and disease-free survival (70% versus 42%; P for both = .06). In general, DM “has a more favorable prognosis,” Dr. Roden said.

Cases and controls were in their mid-60s, on average, and most were men. Ulceration was present in about a quarter of patients. Mitosis was more common in superficial spreading and nodular patients (92% versus 53%; P less than .001), while perineural invasion was more common in DM (40% versus 7%; P less than.001).

Although outcomes were more favorable for DM, previous studies have found a higher rate of sentinel lymph node metastases – above 20% – for DM lesions with mixed, rather than pure, pathology. The 6.3% positive SLNB rate at NYU is more in line with what’s been reported before for pure lesions. The team plans to look into the matter.

There was no outside funding for the work, and Dr. Roden had no disclosures.

[email protected]

SEATTLE – Sentinel lymph node biopsy in patients with head or neck desmoplastic melanoma is positive only 6% of the time, and it doesn’t change the risk of recurrence.

Although sentinel lymph node biopsy (SLNB) is routine in more common forms of cutaneous melanoma, findings from a retrospective case-control study suggest that it’s “not really necessary” for desmoplastic melanoma (DM) of the head or neck, said lead investigator Dylan Roden, MD, of the department of otolaryngology, New York University. General surgeons have pretty much come to that conclusion for DM elsewhere on the body, but it hasn’t been shown before for neck and head lesions, he said.

Dr. Dylan Roden

DM, an invasive form of melanoma in which malignant cells are surrounded by fibrous tissue, accounts for maybe 2% of cutaneous melanomas, with half or so presenting on the head or neck. The reason SLNB is of less use than with other melanomas is that DM “doesn’t often spread through the lymphatics. It’s not that patients won’t ever have metastases, but maybe it will be through the blood. Removing a lymph node won’t necessarily” detect it, Dr. Roden said at the International Conference on Head and Neck Cancer, held by the American Head and Neck Society.

Forgoing SLNB has the added benefit of shaving an hour and a half or more off surgery, which is important since DM patients tend to be older, he added.

The NYU team matched 32 of their cases with 60 controls with more common superficial spreading or nodular melanoma of the head and neck, based on age, gender, ulceration status, and tumor stage. Mean tumor thickness in both groups was more than 4 mm.

SLNB was performed in 16 DM patients (50%) and 36 control patients (60%); it was positive in one DM patient (6.3%) versus 8 of 28 controls with reported results (28.6%).

Eleven DM patients (34%) had a recurrence, which was less frequent then in controls, where 33 patients (55%) had a recurrence (P = .05). “SNLB did not change the risk of overall or regional recurrence” in DM, Dr. Roden said.

Recurrence was more than twice as likely in control patients (odds ratio, 2.33; P = .06). Meanwhile, recurrence in DM was linked to perineural invasion (P = .02), but not ulceration status (P = .12) or mitoses (P = .40).

DM patients also had better 5-year overall survival (79% versus 62%) and disease-free survival (70% versus 42%; P for both = .06). In general, DM “has a more favorable prognosis,” Dr. Roden said.

Cases and controls were in their mid-60s, on average, and most were men. Ulceration was present in about a quarter of patients. Mitosis was more common in superficial spreading and nodular patients (92% versus 53%; P less than .001), while perineural invasion was more common in DM (40% versus 7%; P less than.001).

Although outcomes were more favorable for DM, previous studies have found a higher rate of sentinel lymph node metastases – above 20% – for DM lesions with mixed, rather than pure, pathology. The 6.3% positive SLNB rate at NYU is more in line with what’s been reported before for pure lesions. The team plans to look into the matter.

There was no outside funding for the work, and Dr. Roden had no disclosures.

[email protected]

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Key clinical point: Sentinel lymph node biopsy in patients with head or neck desmoplastic melanoma is positive only 6% of the time, and it doesn’t change the risk of recurrence.

Major finding: SLNB was performed in 16 DM patients (50%) and 36 control patients (60%); it was positive in one DM patient (6.3%) versus 8 of 28 controls with reported results (28.6%).

Data source: Retrospective case-control study with 92 patients

Disclosures: There was no outside funding for the work, and the presenter had no disclosures.

Enhanced Radiation Dermatitis Associated With Concurrent Palliative Radiation and Vemurafenib Therapy

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To the Editor:

Vemurafenib is a selective BRAF inhibitor that was approved by the US Food and Drug Administration (FDA) in August 2011 for the treatment of patients with unresectable or metastatic melanoma with the BRAF V600E mutation as detected by an approved test. Both malignant and nonmalignant cutaneous findings have been well documented in association with vemurafenib, including squamous cell carcinoma, keratoacanthomas, UVA photosensitivity, keratosis pilaris–like eruptions, seborrheic dermatitis, follicular plugging, follicular hyperkeratosis, and eruptive melanocytic nevi.1 As more patients with metastatic melanoma are treated with vemurafenib, the use of concomitant palliative or adjuvant radiation therapy with vemurafenib will inevitably occur in greater frequency. Therefore, it is critical to understand the potential cutaneous side effects of this combination.

A predisposition to enhanced radiation dermatitis has been well described with concurrent use of targeted chemotherapies such as the epidermal growth factor receptor inhibitor cetuximab with radiotherapy.2 We report a case of radiation dermatitis occurring shortly after initiating radiation therapy in a patient on vemurafenib.

A 53-year-old man with initial stage IIIB melanoma, Breslow depth 2.2 mm with histologic ulceration, and a mitotic index of 2/mm2 on the right buttock underwent wide local excision and sentinel lymph node biopsy followed by complete lymph node dissection with a total of 2 of 10 positive lymph nodes. The patient subsequently underwent 1 year of adjuvant high-dose interferon therapy. Four years after his initial presentation he developed metastases to the lungs, pelvis, and both femurs. He was started on oral vemurafenib 960 mg twice daily. Due to painful bony metastases in the pelvis, the patient also was started on concurrent palliative radiation therapy to both femurs, L5 vertebra, and the sacrum 1 day after initiation of vemurafenib. Three days after initiation of radiation therapy at a cumulative radiation dose of 0.75 Gy, the patient developed severe, painful, well-demarcated, erythematous plaques in the anterior and posterior pelvic distribution overlying the radiation field (Figure 1) that subsequently evolved to eroded desquamative plaques with copious transudate. The patient also developed hyperkeratotic papules on the chest and thighs consistent with the keratosis pilaris–like eruptions associated with vemurafenib therapy.1 Five months later the patient developed worsening neurologic symptoms, and magnetic resonance imaging of the brain revealed multiple brain metastases. Given his disease progression, vemurafenib was discontinued. Ten days later, the patient underwent palliative whole-brain radiation therapy. He received a total dose of 3.25 Gy to the whole brain without any cutaneous sequelae.

Figure 1. Radiation dermatitis of the buttocks (A), right side of the groin (B), and left side of the groin (C) while on vemurafenib.

The pathophysiology of radiation dermatitis is caused by a dose-dependent loss of basal and endothelial cells following irradiation.3 If surviving basal cells are able to repopulate the basal monolayer, normal skin barrier function is preserved. Dose tolerance is exceeded when cell loss without replacement occurs, resulting in necrosis and clinical evidence of radiation dermatitis, which is characterized by painful erythema or hyperpigmentation followed by desquamation and skin necrosis. In general, occurrence and severity of radiation dermatitis when radiation therapy is used alone in the absence of concurrent chemotherapy is dose dependent, with cutaneous evidence of radiation dermatitis occurring at doses ranging from as low as 2 Gy but most commonly 5 to 10 Gy.4 A report of radiation recall dermatitis in 2 patients who received vemurafenib after completing a full course of radiotherapy5 supports the hypothesis that vemurafenib is a radiosensitizing medication. Enhanced radiation dermatitis was reported in a single case of a patient on vemurafenib who developed radiation dermatitis after completing 3.25 Gy of radiation to the lumbar spine. Although this case likely depicted enhanced radiation dermatitis secondary to concurrent vemurafenib use, it was inconclusive whether vemurafenib contributed to the cutaneous effect, as the patient developed a cutaneous skin reaction 1 week after receiving a cumulative radiation dose of 3.25 Gy, a level at which radiation alone has been shown to cause skin toxicity.6 In our patient, cutaneous manifestations were noted 3 days after initiation of radiation treatment, at which point he had received a total radiation dose of 0.75 Gy, which is well below the threshold commonly recognized to cause radiation-induced skin toxicities. In addition, rechallenge in this patient with higher-dose radiotherapy while off of vemurafenib treatment led to no skin toxicity, despite the common side effects of whole-brain radiation therapy including radiation dermatitis and alopecia.7

 

 

The exact mechanism of increased radiosensitivity caused by targeted chemotherapies such as cetuximab and vemurafenib is unclear. One possible explanation is that the drug interferes with the mitogen-activated protein kinase (MAPK) pathway, which plays a crucial role in controlling cell survival and regeneration following radiation exposure.8 Disruption of this signaling pathway through targeted therapies leads to impaired keratinocyte cell survival and recovery, and thus may enhance susceptibility to radiation-induced skin injury (Figure 2). In vivo studies have demonstrated that the epidermal growth factor receptor is activated following UV irradiation in human keratinocytes, leading to activation of the downstream MAPK signal transduction pathway required for cellular proliferation mediated via the RAF family of proteins.9,10 Further supporting the importance of this pathway in keratinocyte survival and recovery are findings that somatic deletion of BRAF in fibroblasts results in decreased growth factor–induced MAPK activation and enhanced apoptosis,8 whereas activated BRAF has been shown to exert protective effects against oxidative stress as well as tumorigenesis.11 The observation that mutant BRAF melanoma cells demonstrated increased radiosensitivity following BRAF inhibition with vemurafenib12 is consistent with our hypothesis that increased radiosensitivity occurs when signal transduction mediated by MAPK pathway is blocked, thereby inhibiting cell survival. As a result, radiation dermatitis is likely to occur more frequently and at a lower dose when signaling pathways upstream in the MAPK pathway required for keratinocyte regeneration, such as epidermal growth factor receptor and BRAF, are inhibited by targeted therapies. This hypothesis supports the observation that patients on medications that inhibit these signaling pathways, such as cetuximab and vemurafenib, develop enhanced sensitivity to both UV radiation and radiation therapy.

Figure 2. Radiosensitizing chemotherapeutic agents targeting the mitogen-activated protein kinase (MAPK) signaling pathway. EGFR indicates epidermal growth factor receptor; P, active, phosphorylated form of EGFR.

We report a case of enhanced radiation dermatitis occurring at a total dose of 0.75 Gy of radiotherapy, well below the threshold commonly recognized to cause radiation-induced skin toxicities. Our observation suggests that vemurafenib likely acts as a radiosensitizing agent that notably decreases the threshold for radiotherapy-related skin toxicities. Furthermore, the radiosensitizing effect of vemurafenib appears to be transient, as our patient showed no evidence of any skin reaction to subsequent radiation treatment soon after vemurafenib was discontinued. As more patients with metastatic melanoma are treated with vemurafenib, the combination of palliative or adjuvant radiation therapy with vemurafenib will likely be used more frequently. Caution should be exercised in patients on vemurafenib who receive concurrent radiotherapy, even at low radiation doses.
References
  1. Huang V, Hepper D, Anadkat M, et al. Cutaneous toxic effects associated with vemurafenib and inhibition of the BRAF pathway. Arch Dermatol. 2012;148:628-633.
  2. Studer G, Brown M, Dalgueiro E, et al. Grade 3/4 dermatitis in head and neck cancer patients treated with concurrent cetuximab and IMRT. Int J Radiat Oncol Biol Phys. 2011;81:110-117.
  3. Archambeau JO, Pezner R, Wasserman T. Pathophysiology of irradiated skin and breast. Int J Radiat Oncol Biol Phys. 1995;31:1171-1185.
  4. Balter S, Hopewell JW, Miller DL, et al. Fluoroscopically guided interventional procedures: a review of radiation effects on patients’ skin and hair. Radiology. 2010;254:326-341.
  5. Boussemart L, Boivin C, Claveau J, et al. Vemurafenib and radiosensitization. JAMA Dermatol. 2013;149:855-857.
  6. Churilla TM, Chowdhry VK, Pan D, et al. Radiation-induced dermatitis with vemurafenib therapy. Pract Radiat Oncol. 2013;3:e195-e198.
  7. Anker CJ, Grossmann KF, Atkins MB, et al. Avoiding severe toxicity from combined BRAF inhibitor and radiation treatment: consensus guidelines from the Eastern Cooperative Oncology Group (ECOG). Int J Radiat Oncol Biol Phys. 2016;95:632-646.
  8. Dent P, Yacoub A, Fisher PB, et al. MAPK pathways in radiation responses. Oncogene. 2003;22:5885-5896.
  9. Cao C, Lus S, Jiang Q, et al. EGFR activation confers protections against UV-induced apoptosis in cultured mouse skin dendritic cells. Cell Signal. 2008;20:1830-1838.
  10. Xu Y, Shao Y, Zhou J, et al. Ultraviolet irradiation-induces epidermal growth factor receptor (EGFR) nuclear translocation in human keratinocytes. J Cell Biochem. 2009;107:873-880.
  11. Valerie K, Yacoub A, Hagan M, et al. Radiation-induced cell signaling: inside-out and outside-in. Mol Cancer Ther. 2007;6:789-801.
  12. Sambade M, Peters E, Thomas N, et al. Melanoma cells show a heterogeneous range of sensitivity to ionizing radiation and are radiosensitized by inhibition of B-RAF with PLX-4032. Radiother Oncol. 2011;98:394-399.
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All from the Department of Dermatology, Stanford University Medical Center and Cancer Institute, California. Dr. Swetter also is from Dermatology Service, VA Palo Alto Health Care System, California.

The authors report no conflict of interest.

Correspondence: Bernice Y. Kwong, MD, Department of Dermatology, Stanford University Medical Center and Cancer Institute, 780 Welch Rd, CJ220-C21, Palo Alto, CA 94304-5779 ([email protected]).

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All from the Department of Dermatology, Stanford University Medical Center and Cancer Institute, California. Dr. Swetter also is from Dermatology Service, VA Palo Alto Health Care System, California.

The authors report no conflict of interest.

Correspondence: Bernice Y. Kwong, MD, Department of Dermatology, Stanford University Medical Center and Cancer Institute, 780 Welch Rd, CJ220-C21, Palo Alto, CA 94304-5779 ([email protected]).

Author and Disclosure Information

All from the Department of Dermatology, Stanford University Medical Center and Cancer Institute, California. Dr. Swetter also is from Dermatology Service, VA Palo Alto Health Care System, California.

The authors report no conflict of interest.

Correspondence: Bernice Y. Kwong, MD, Department of Dermatology, Stanford University Medical Center and Cancer Institute, 780 Welch Rd, CJ220-C21, Palo Alto, CA 94304-5779 ([email protected]).

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To the Editor:

Vemurafenib is a selective BRAF inhibitor that was approved by the US Food and Drug Administration (FDA) in August 2011 for the treatment of patients with unresectable or metastatic melanoma with the BRAF V600E mutation as detected by an approved test. Both malignant and nonmalignant cutaneous findings have been well documented in association with vemurafenib, including squamous cell carcinoma, keratoacanthomas, UVA photosensitivity, keratosis pilaris–like eruptions, seborrheic dermatitis, follicular plugging, follicular hyperkeratosis, and eruptive melanocytic nevi.1 As more patients with metastatic melanoma are treated with vemurafenib, the use of concomitant palliative or adjuvant radiation therapy with vemurafenib will inevitably occur in greater frequency. Therefore, it is critical to understand the potential cutaneous side effects of this combination.

A predisposition to enhanced radiation dermatitis has been well described with concurrent use of targeted chemotherapies such as the epidermal growth factor receptor inhibitor cetuximab with radiotherapy.2 We report a case of radiation dermatitis occurring shortly after initiating radiation therapy in a patient on vemurafenib.

A 53-year-old man with initial stage IIIB melanoma, Breslow depth 2.2 mm with histologic ulceration, and a mitotic index of 2/mm2 on the right buttock underwent wide local excision and sentinel lymph node biopsy followed by complete lymph node dissection with a total of 2 of 10 positive lymph nodes. The patient subsequently underwent 1 year of adjuvant high-dose interferon therapy. Four years after his initial presentation he developed metastases to the lungs, pelvis, and both femurs. He was started on oral vemurafenib 960 mg twice daily. Due to painful bony metastases in the pelvis, the patient also was started on concurrent palliative radiation therapy to both femurs, L5 vertebra, and the sacrum 1 day after initiation of vemurafenib. Three days after initiation of radiation therapy at a cumulative radiation dose of 0.75 Gy, the patient developed severe, painful, well-demarcated, erythematous plaques in the anterior and posterior pelvic distribution overlying the radiation field (Figure 1) that subsequently evolved to eroded desquamative plaques with copious transudate. The patient also developed hyperkeratotic papules on the chest and thighs consistent with the keratosis pilaris–like eruptions associated with vemurafenib therapy.1 Five months later the patient developed worsening neurologic symptoms, and magnetic resonance imaging of the brain revealed multiple brain metastases. Given his disease progression, vemurafenib was discontinued. Ten days later, the patient underwent palliative whole-brain radiation therapy. He received a total dose of 3.25 Gy to the whole brain without any cutaneous sequelae.

Figure 1. Radiation dermatitis of the buttocks (A), right side of the groin (B), and left side of the groin (C) while on vemurafenib.

The pathophysiology of radiation dermatitis is caused by a dose-dependent loss of basal and endothelial cells following irradiation.3 If surviving basal cells are able to repopulate the basal monolayer, normal skin barrier function is preserved. Dose tolerance is exceeded when cell loss without replacement occurs, resulting in necrosis and clinical evidence of radiation dermatitis, which is characterized by painful erythema or hyperpigmentation followed by desquamation and skin necrosis. In general, occurrence and severity of radiation dermatitis when radiation therapy is used alone in the absence of concurrent chemotherapy is dose dependent, with cutaneous evidence of radiation dermatitis occurring at doses ranging from as low as 2 Gy but most commonly 5 to 10 Gy.4 A report of radiation recall dermatitis in 2 patients who received vemurafenib after completing a full course of radiotherapy5 supports the hypothesis that vemurafenib is a radiosensitizing medication. Enhanced radiation dermatitis was reported in a single case of a patient on vemurafenib who developed radiation dermatitis after completing 3.25 Gy of radiation to the lumbar spine. Although this case likely depicted enhanced radiation dermatitis secondary to concurrent vemurafenib use, it was inconclusive whether vemurafenib contributed to the cutaneous effect, as the patient developed a cutaneous skin reaction 1 week after receiving a cumulative radiation dose of 3.25 Gy, a level at which radiation alone has been shown to cause skin toxicity.6 In our patient, cutaneous manifestations were noted 3 days after initiation of radiation treatment, at which point he had received a total radiation dose of 0.75 Gy, which is well below the threshold commonly recognized to cause radiation-induced skin toxicities. In addition, rechallenge in this patient with higher-dose radiotherapy while off of vemurafenib treatment led to no skin toxicity, despite the common side effects of whole-brain radiation therapy including radiation dermatitis and alopecia.7

 

 

The exact mechanism of increased radiosensitivity caused by targeted chemotherapies such as cetuximab and vemurafenib is unclear. One possible explanation is that the drug interferes with the mitogen-activated protein kinase (MAPK) pathway, which plays a crucial role in controlling cell survival and regeneration following radiation exposure.8 Disruption of this signaling pathway through targeted therapies leads to impaired keratinocyte cell survival and recovery, and thus may enhance susceptibility to radiation-induced skin injury (Figure 2). In vivo studies have demonstrated that the epidermal growth factor receptor is activated following UV irradiation in human keratinocytes, leading to activation of the downstream MAPK signal transduction pathway required for cellular proliferation mediated via the RAF family of proteins.9,10 Further supporting the importance of this pathway in keratinocyte survival and recovery are findings that somatic deletion of BRAF in fibroblasts results in decreased growth factor–induced MAPK activation and enhanced apoptosis,8 whereas activated BRAF has been shown to exert protective effects against oxidative stress as well as tumorigenesis.11 The observation that mutant BRAF melanoma cells demonstrated increased radiosensitivity following BRAF inhibition with vemurafenib12 is consistent with our hypothesis that increased radiosensitivity occurs when signal transduction mediated by MAPK pathway is blocked, thereby inhibiting cell survival. As a result, radiation dermatitis is likely to occur more frequently and at a lower dose when signaling pathways upstream in the MAPK pathway required for keratinocyte regeneration, such as epidermal growth factor receptor and BRAF, are inhibited by targeted therapies. This hypothesis supports the observation that patients on medications that inhibit these signaling pathways, such as cetuximab and vemurafenib, develop enhanced sensitivity to both UV radiation and radiation therapy.

Figure 2. Radiosensitizing chemotherapeutic agents targeting the mitogen-activated protein kinase (MAPK) signaling pathway. EGFR indicates epidermal growth factor receptor; P, active, phosphorylated form of EGFR.

We report a case of enhanced radiation dermatitis occurring at a total dose of 0.75 Gy of radiotherapy, well below the threshold commonly recognized to cause radiation-induced skin toxicities. Our observation suggests that vemurafenib likely acts as a radiosensitizing agent that notably decreases the threshold for radiotherapy-related skin toxicities. Furthermore, the radiosensitizing effect of vemurafenib appears to be transient, as our patient showed no evidence of any skin reaction to subsequent radiation treatment soon after vemurafenib was discontinued. As more patients with metastatic melanoma are treated with vemurafenib, the combination of palliative or adjuvant radiation therapy with vemurafenib will likely be used more frequently. Caution should be exercised in patients on vemurafenib who receive concurrent radiotherapy, even at low radiation doses.

To the Editor:

Vemurafenib is a selective BRAF inhibitor that was approved by the US Food and Drug Administration (FDA) in August 2011 for the treatment of patients with unresectable or metastatic melanoma with the BRAF V600E mutation as detected by an approved test. Both malignant and nonmalignant cutaneous findings have been well documented in association with vemurafenib, including squamous cell carcinoma, keratoacanthomas, UVA photosensitivity, keratosis pilaris–like eruptions, seborrheic dermatitis, follicular plugging, follicular hyperkeratosis, and eruptive melanocytic nevi.1 As more patients with metastatic melanoma are treated with vemurafenib, the use of concomitant palliative or adjuvant radiation therapy with vemurafenib will inevitably occur in greater frequency. Therefore, it is critical to understand the potential cutaneous side effects of this combination.

A predisposition to enhanced radiation dermatitis has been well described with concurrent use of targeted chemotherapies such as the epidermal growth factor receptor inhibitor cetuximab with radiotherapy.2 We report a case of radiation dermatitis occurring shortly after initiating radiation therapy in a patient on vemurafenib.

A 53-year-old man with initial stage IIIB melanoma, Breslow depth 2.2 mm with histologic ulceration, and a mitotic index of 2/mm2 on the right buttock underwent wide local excision and sentinel lymph node biopsy followed by complete lymph node dissection with a total of 2 of 10 positive lymph nodes. The patient subsequently underwent 1 year of adjuvant high-dose interferon therapy. Four years after his initial presentation he developed metastases to the lungs, pelvis, and both femurs. He was started on oral vemurafenib 960 mg twice daily. Due to painful bony metastases in the pelvis, the patient also was started on concurrent palliative radiation therapy to both femurs, L5 vertebra, and the sacrum 1 day after initiation of vemurafenib. Three days after initiation of radiation therapy at a cumulative radiation dose of 0.75 Gy, the patient developed severe, painful, well-demarcated, erythematous plaques in the anterior and posterior pelvic distribution overlying the radiation field (Figure 1) that subsequently evolved to eroded desquamative plaques with copious transudate. The patient also developed hyperkeratotic papules on the chest and thighs consistent with the keratosis pilaris–like eruptions associated with vemurafenib therapy.1 Five months later the patient developed worsening neurologic symptoms, and magnetic resonance imaging of the brain revealed multiple brain metastases. Given his disease progression, vemurafenib was discontinued. Ten days later, the patient underwent palliative whole-brain radiation therapy. He received a total dose of 3.25 Gy to the whole brain without any cutaneous sequelae.

Figure 1. Radiation dermatitis of the buttocks (A), right side of the groin (B), and left side of the groin (C) while on vemurafenib.

The pathophysiology of radiation dermatitis is caused by a dose-dependent loss of basal and endothelial cells following irradiation.3 If surviving basal cells are able to repopulate the basal monolayer, normal skin barrier function is preserved. Dose tolerance is exceeded when cell loss without replacement occurs, resulting in necrosis and clinical evidence of radiation dermatitis, which is characterized by painful erythema or hyperpigmentation followed by desquamation and skin necrosis. In general, occurrence and severity of radiation dermatitis when radiation therapy is used alone in the absence of concurrent chemotherapy is dose dependent, with cutaneous evidence of radiation dermatitis occurring at doses ranging from as low as 2 Gy but most commonly 5 to 10 Gy.4 A report of radiation recall dermatitis in 2 patients who received vemurafenib after completing a full course of radiotherapy5 supports the hypothesis that vemurafenib is a radiosensitizing medication. Enhanced radiation dermatitis was reported in a single case of a patient on vemurafenib who developed radiation dermatitis after completing 3.25 Gy of radiation to the lumbar spine. Although this case likely depicted enhanced radiation dermatitis secondary to concurrent vemurafenib use, it was inconclusive whether vemurafenib contributed to the cutaneous effect, as the patient developed a cutaneous skin reaction 1 week after receiving a cumulative radiation dose of 3.25 Gy, a level at which radiation alone has been shown to cause skin toxicity.6 In our patient, cutaneous manifestations were noted 3 days after initiation of radiation treatment, at which point he had received a total radiation dose of 0.75 Gy, which is well below the threshold commonly recognized to cause radiation-induced skin toxicities. In addition, rechallenge in this patient with higher-dose radiotherapy while off of vemurafenib treatment led to no skin toxicity, despite the common side effects of whole-brain radiation therapy including radiation dermatitis and alopecia.7

 

 

The exact mechanism of increased radiosensitivity caused by targeted chemotherapies such as cetuximab and vemurafenib is unclear. One possible explanation is that the drug interferes with the mitogen-activated protein kinase (MAPK) pathway, which plays a crucial role in controlling cell survival and regeneration following radiation exposure.8 Disruption of this signaling pathway through targeted therapies leads to impaired keratinocyte cell survival and recovery, and thus may enhance susceptibility to radiation-induced skin injury (Figure 2). In vivo studies have demonstrated that the epidermal growth factor receptor is activated following UV irradiation in human keratinocytes, leading to activation of the downstream MAPK signal transduction pathway required for cellular proliferation mediated via the RAF family of proteins.9,10 Further supporting the importance of this pathway in keratinocyte survival and recovery are findings that somatic deletion of BRAF in fibroblasts results in decreased growth factor–induced MAPK activation and enhanced apoptosis,8 whereas activated BRAF has been shown to exert protective effects against oxidative stress as well as tumorigenesis.11 The observation that mutant BRAF melanoma cells demonstrated increased radiosensitivity following BRAF inhibition with vemurafenib12 is consistent with our hypothesis that increased radiosensitivity occurs when signal transduction mediated by MAPK pathway is blocked, thereby inhibiting cell survival. As a result, radiation dermatitis is likely to occur more frequently and at a lower dose when signaling pathways upstream in the MAPK pathway required for keratinocyte regeneration, such as epidermal growth factor receptor and BRAF, are inhibited by targeted therapies. This hypothesis supports the observation that patients on medications that inhibit these signaling pathways, such as cetuximab and vemurafenib, develop enhanced sensitivity to both UV radiation and radiation therapy.

Figure 2. Radiosensitizing chemotherapeutic agents targeting the mitogen-activated protein kinase (MAPK) signaling pathway. EGFR indicates epidermal growth factor receptor; P, active, phosphorylated form of EGFR.

We report a case of enhanced radiation dermatitis occurring at a total dose of 0.75 Gy of radiotherapy, well below the threshold commonly recognized to cause radiation-induced skin toxicities. Our observation suggests that vemurafenib likely acts as a radiosensitizing agent that notably decreases the threshold for radiotherapy-related skin toxicities. Furthermore, the radiosensitizing effect of vemurafenib appears to be transient, as our patient showed no evidence of any skin reaction to subsequent radiation treatment soon after vemurafenib was discontinued. As more patients with metastatic melanoma are treated with vemurafenib, the combination of palliative or adjuvant radiation therapy with vemurafenib will likely be used more frequently. Caution should be exercised in patients on vemurafenib who receive concurrent radiotherapy, even at low radiation doses.
References
  1. Huang V, Hepper D, Anadkat M, et al. Cutaneous toxic effects associated with vemurafenib and inhibition of the BRAF pathway. Arch Dermatol. 2012;148:628-633.
  2. Studer G, Brown M, Dalgueiro E, et al. Grade 3/4 dermatitis in head and neck cancer patients treated with concurrent cetuximab and IMRT. Int J Radiat Oncol Biol Phys. 2011;81:110-117.
  3. Archambeau JO, Pezner R, Wasserman T. Pathophysiology of irradiated skin and breast. Int J Radiat Oncol Biol Phys. 1995;31:1171-1185.
  4. Balter S, Hopewell JW, Miller DL, et al. Fluoroscopically guided interventional procedures: a review of radiation effects on patients’ skin and hair. Radiology. 2010;254:326-341.
  5. Boussemart L, Boivin C, Claveau J, et al. Vemurafenib and radiosensitization. JAMA Dermatol. 2013;149:855-857.
  6. Churilla TM, Chowdhry VK, Pan D, et al. Radiation-induced dermatitis with vemurafenib therapy. Pract Radiat Oncol. 2013;3:e195-e198.
  7. Anker CJ, Grossmann KF, Atkins MB, et al. Avoiding severe toxicity from combined BRAF inhibitor and radiation treatment: consensus guidelines from the Eastern Cooperative Oncology Group (ECOG). Int J Radiat Oncol Biol Phys. 2016;95:632-646.
  8. Dent P, Yacoub A, Fisher PB, et al. MAPK pathways in radiation responses. Oncogene. 2003;22:5885-5896.
  9. Cao C, Lus S, Jiang Q, et al. EGFR activation confers protections against UV-induced apoptosis in cultured mouse skin dendritic cells. Cell Signal. 2008;20:1830-1838.
  10. Xu Y, Shao Y, Zhou J, et al. Ultraviolet irradiation-induces epidermal growth factor receptor (EGFR) nuclear translocation in human keratinocytes. J Cell Biochem. 2009;107:873-880.
  11. Valerie K, Yacoub A, Hagan M, et al. Radiation-induced cell signaling: inside-out and outside-in. Mol Cancer Ther. 2007;6:789-801.
  12. Sambade M, Peters E, Thomas N, et al. Melanoma cells show a heterogeneous range of sensitivity to ionizing radiation and are radiosensitized by inhibition of B-RAF with PLX-4032. Radiother Oncol. 2011;98:394-399.
References
  1. Huang V, Hepper D, Anadkat M, et al. Cutaneous toxic effects associated with vemurafenib and inhibition of the BRAF pathway. Arch Dermatol. 2012;148:628-633.
  2. Studer G, Brown M, Dalgueiro E, et al. Grade 3/4 dermatitis in head and neck cancer patients treated with concurrent cetuximab and IMRT. Int J Radiat Oncol Biol Phys. 2011;81:110-117.
  3. Archambeau JO, Pezner R, Wasserman T. Pathophysiology of irradiated skin and breast. Int J Radiat Oncol Biol Phys. 1995;31:1171-1185.
  4. Balter S, Hopewell JW, Miller DL, et al. Fluoroscopically guided interventional procedures: a review of radiation effects on patients’ skin and hair. Radiology. 2010;254:326-341.
  5. Boussemart L, Boivin C, Claveau J, et al. Vemurafenib and radiosensitization. JAMA Dermatol. 2013;149:855-857.
  6. Churilla TM, Chowdhry VK, Pan D, et al. Radiation-induced dermatitis with vemurafenib therapy. Pract Radiat Oncol. 2013;3:e195-e198.
  7. Anker CJ, Grossmann KF, Atkins MB, et al. Avoiding severe toxicity from combined BRAF inhibitor and radiation treatment: consensus guidelines from the Eastern Cooperative Oncology Group (ECOG). Int J Radiat Oncol Biol Phys. 2016;95:632-646.
  8. Dent P, Yacoub A, Fisher PB, et al. MAPK pathways in radiation responses. Oncogene. 2003;22:5885-5896.
  9. Cao C, Lus S, Jiang Q, et al. EGFR activation confers protections against UV-induced apoptosis in cultured mouse skin dendritic cells. Cell Signal. 2008;20:1830-1838.
  10. Xu Y, Shao Y, Zhou J, et al. Ultraviolet irradiation-induces epidermal growth factor receptor (EGFR) nuclear translocation in human keratinocytes. J Cell Biochem. 2009;107:873-880.
  11. Valerie K, Yacoub A, Hagan M, et al. Radiation-induced cell signaling: inside-out and outside-in. Mol Cancer Ther. 2007;6:789-801.
  12. Sambade M, Peters E, Thomas N, et al. Melanoma cells show a heterogeneous range of sensitivity to ionizing radiation and are radiosensitized by inhibition of B-RAF with PLX-4032. Radiother Oncol. 2011;98:394-399.
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  • Given the increased frequency of palliative and adjuvant radiation therapy in patients with metastatic melanoma, it is critical to understand the potential cutaneous side effects of vemurafenib when used in conjunction with radiotherapy.
  • Clinicians should be aware of the increased risk for severe radiation dermatitis in patients on vemurafenib who are receiving concurrent palliative radiation therapy.
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Certain skin cancers respond to nonsurgical treatments

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BOSTON – Surgery is the standard of care for most skin cancers, but nonsurgical and adjuvant treatments can be good options for certain skin cancers when surgery would be neither curative nor feasible, according to Anthony Rossi, MD.

“Whether you’re treating a superficial basal cell or superficial squamous cell carcinoma, I think first and foremost, if you’re going to use nonsurgical treatment options, it’s important to have a good biopsy diagnosis,” Dr. Rossi said at the American Academy of Dermatology summer meeting. He also advised that the biopsy capture the entire lesion or a good portion of it to get a good representation. “You don’t want to be surprised by any hiding, high-risk subtypes,” said Dr. Rossi, of the Memorial Sloan Kettering Cancer Center in New York.

Dr. Anthony Rossi

Deciding on a nonsurgical treatment option should be based on knowing the patient. For example, know the patient’s concerns about cosmetic deformities, willingness to undergo surgery or not, and ability and willingness to do follow-up self-care.

For superficial basal cell or squamous cell carcinomas in situ and even lentigo maligna in situ not amenable to surgery, imiquimod may be an appropriate treatment. Dr. Rossi said his practice is to use it in an incremental fashion, starting with application five times per week, going to every day if there is no response after 1 to 2 weeks. If the response remains inadequate, he recommended adding a topical retinoid, such as tazarotene, in an effort to increase penetration.

For basal cell carcinomas and squamous cell carcinoma in situ, he uses imiquimod for a total of 6 to 8 weeks, starting from the time of the first reaction. For melanoma in situ, he uses it for more than 60 applications (12 weeks).

To show patients where they should be applying any topical treatment, Dr. Rossi marks the skin, photographs it, and prints out a picture for the patient. Sometimes he uses the patient’s phone to take the picture. For a basal cell or squamous cell carcinoma in situ, he indicates an area at least 5 to 10 mm beyond the margin of the tumor. The area is even larger for melanomas.

Dr. Rossi studies confocal microscopy to detect skin cancers. He uses it before treating a lesion to define the clinical boundaries of the lesion and the boundaries for the nonsurgical treatments, and then he uses it on follow up to look for any recurrences.

New anti-tumor agents

Two oral inhibitors of the sonic hedgehog pathway have been approved within the past 5 years for locally advanced or metastatic basal cell carcinomas. “In the right person, they can be quite beneficial if surgery would leave them with a very large cosmetic deformity or if surgery would be not curative,” Dr. Rossi said. “We’re seeing good results” with acceptable adverse events, specifically taste disturbances, muscle cramps, and hair loss. The first such drug, vismodegib (Erivedge), was approved in 2012, and sonidegib (Odomzo) came on the market about 1 year ago.

Besides oral agents, photodynamic therapy (PDT) with photosensitizers are another option for certain skin tumors. Dr. Rossi said his practice is to keep the treatment room fairly warm to assure good blood flow to the skin and thus good penetration of the drug. Because PDT acts by generating singlet oxygen to kill tumors, good blood flow to the tumor is necessary. To minimize discomfort, he uses pretreatment acetaminophen if patients can take it. After a skin reaction occurs, cool compresses are used, along with dilute acetic acid soaks on crusted or scaling lesions in an effort to prevent infection.

And while these treatments can produce quite angry-looking lesions in the short term, very good healing usually occurs if patients are diligent about wound care. However, Dr. Rossi cautioned that they may need “more hand holding with these nonsurgical treatments, because it is a longer duration of treatment.”

In general for counseling patients on nonsurgical treatments, Dr. Rossi said it is advisable to have good pretreatment and post-treatment plans. “They have to know that they will need to be following up to make sure that there is no recurrence,” he said. “We don’t have clear surgical margins if we’re using these topical treatments, so we have to make sure that they have good, constant follow-up.”

Dr. Rossi reported consulting relationships with Merz, DynaMed, and Novartis.

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BOSTON – Surgery is the standard of care for most skin cancers, but nonsurgical and adjuvant treatments can be good options for certain skin cancers when surgery would be neither curative nor feasible, according to Anthony Rossi, MD.

“Whether you’re treating a superficial basal cell or superficial squamous cell carcinoma, I think first and foremost, if you’re going to use nonsurgical treatment options, it’s important to have a good biopsy diagnosis,” Dr. Rossi said at the American Academy of Dermatology summer meeting. He also advised that the biopsy capture the entire lesion or a good portion of it to get a good representation. “You don’t want to be surprised by any hiding, high-risk subtypes,” said Dr. Rossi, of the Memorial Sloan Kettering Cancer Center in New York.

Dr. Anthony Rossi

Deciding on a nonsurgical treatment option should be based on knowing the patient. For example, know the patient’s concerns about cosmetic deformities, willingness to undergo surgery or not, and ability and willingness to do follow-up self-care.

For superficial basal cell or squamous cell carcinomas in situ and even lentigo maligna in situ not amenable to surgery, imiquimod may be an appropriate treatment. Dr. Rossi said his practice is to use it in an incremental fashion, starting with application five times per week, going to every day if there is no response after 1 to 2 weeks. If the response remains inadequate, he recommended adding a topical retinoid, such as tazarotene, in an effort to increase penetration.

For basal cell carcinomas and squamous cell carcinoma in situ, he uses imiquimod for a total of 6 to 8 weeks, starting from the time of the first reaction. For melanoma in situ, he uses it for more than 60 applications (12 weeks).

To show patients where they should be applying any topical treatment, Dr. Rossi marks the skin, photographs it, and prints out a picture for the patient. Sometimes he uses the patient’s phone to take the picture. For a basal cell or squamous cell carcinoma in situ, he indicates an area at least 5 to 10 mm beyond the margin of the tumor. The area is even larger for melanomas.

Dr. Rossi studies confocal microscopy to detect skin cancers. He uses it before treating a lesion to define the clinical boundaries of the lesion and the boundaries for the nonsurgical treatments, and then he uses it on follow up to look for any recurrences.

New anti-tumor agents

Two oral inhibitors of the sonic hedgehog pathway have been approved within the past 5 years for locally advanced or metastatic basal cell carcinomas. “In the right person, they can be quite beneficial if surgery would leave them with a very large cosmetic deformity or if surgery would be not curative,” Dr. Rossi said. “We’re seeing good results” with acceptable adverse events, specifically taste disturbances, muscle cramps, and hair loss. The first such drug, vismodegib (Erivedge), was approved in 2012, and sonidegib (Odomzo) came on the market about 1 year ago.

Besides oral agents, photodynamic therapy (PDT) with photosensitizers are another option for certain skin tumors. Dr. Rossi said his practice is to keep the treatment room fairly warm to assure good blood flow to the skin and thus good penetration of the drug. Because PDT acts by generating singlet oxygen to kill tumors, good blood flow to the tumor is necessary. To minimize discomfort, he uses pretreatment acetaminophen if patients can take it. After a skin reaction occurs, cool compresses are used, along with dilute acetic acid soaks on crusted or scaling lesions in an effort to prevent infection.

And while these treatments can produce quite angry-looking lesions in the short term, very good healing usually occurs if patients are diligent about wound care. However, Dr. Rossi cautioned that they may need “more hand holding with these nonsurgical treatments, because it is a longer duration of treatment.”

In general for counseling patients on nonsurgical treatments, Dr. Rossi said it is advisable to have good pretreatment and post-treatment plans. “They have to know that they will need to be following up to make sure that there is no recurrence,” he said. “We don’t have clear surgical margins if we’re using these topical treatments, so we have to make sure that they have good, constant follow-up.”

Dr. Rossi reported consulting relationships with Merz, DynaMed, and Novartis.

BOSTON – Surgery is the standard of care for most skin cancers, but nonsurgical and adjuvant treatments can be good options for certain skin cancers when surgery would be neither curative nor feasible, according to Anthony Rossi, MD.

“Whether you’re treating a superficial basal cell or superficial squamous cell carcinoma, I think first and foremost, if you’re going to use nonsurgical treatment options, it’s important to have a good biopsy diagnosis,” Dr. Rossi said at the American Academy of Dermatology summer meeting. He also advised that the biopsy capture the entire lesion or a good portion of it to get a good representation. “You don’t want to be surprised by any hiding, high-risk subtypes,” said Dr. Rossi, of the Memorial Sloan Kettering Cancer Center in New York.

Dr. Anthony Rossi

Deciding on a nonsurgical treatment option should be based on knowing the patient. For example, know the patient’s concerns about cosmetic deformities, willingness to undergo surgery or not, and ability and willingness to do follow-up self-care.

For superficial basal cell or squamous cell carcinomas in situ and even lentigo maligna in situ not amenable to surgery, imiquimod may be an appropriate treatment. Dr. Rossi said his practice is to use it in an incremental fashion, starting with application five times per week, going to every day if there is no response after 1 to 2 weeks. If the response remains inadequate, he recommended adding a topical retinoid, such as tazarotene, in an effort to increase penetration.

For basal cell carcinomas and squamous cell carcinoma in situ, he uses imiquimod for a total of 6 to 8 weeks, starting from the time of the first reaction. For melanoma in situ, he uses it for more than 60 applications (12 weeks).

To show patients where they should be applying any topical treatment, Dr. Rossi marks the skin, photographs it, and prints out a picture for the patient. Sometimes he uses the patient’s phone to take the picture. For a basal cell or squamous cell carcinoma in situ, he indicates an area at least 5 to 10 mm beyond the margin of the tumor. The area is even larger for melanomas.

Dr. Rossi studies confocal microscopy to detect skin cancers. He uses it before treating a lesion to define the clinical boundaries of the lesion and the boundaries for the nonsurgical treatments, and then he uses it on follow up to look for any recurrences.

New anti-tumor agents

Two oral inhibitors of the sonic hedgehog pathway have been approved within the past 5 years for locally advanced or metastatic basal cell carcinomas. “In the right person, they can be quite beneficial if surgery would leave them with a very large cosmetic deformity or if surgery would be not curative,” Dr. Rossi said. “We’re seeing good results” with acceptable adverse events, specifically taste disturbances, muscle cramps, and hair loss. The first such drug, vismodegib (Erivedge), was approved in 2012, and sonidegib (Odomzo) came on the market about 1 year ago.

Besides oral agents, photodynamic therapy (PDT) with photosensitizers are another option for certain skin tumors. Dr. Rossi said his practice is to keep the treatment room fairly warm to assure good blood flow to the skin and thus good penetration of the drug. Because PDT acts by generating singlet oxygen to kill tumors, good blood flow to the tumor is necessary. To minimize discomfort, he uses pretreatment acetaminophen if patients can take it. After a skin reaction occurs, cool compresses are used, along with dilute acetic acid soaks on crusted or scaling lesions in an effort to prevent infection.

And while these treatments can produce quite angry-looking lesions in the short term, very good healing usually occurs if patients are diligent about wound care. However, Dr. Rossi cautioned that they may need “more hand holding with these nonsurgical treatments, because it is a longer duration of treatment.”

In general for counseling patients on nonsurgical treatments, Dr. Rossi said it is advisable to have good pretreatment and post-treatment plans. “They have to know that they will need to be following up to make sure that there is no recurrence,” he said. “We don’t have clear surgical margins if we’re using these topical treatments, so we have to make sure that they have good, constant follow-up.”

Dr. Rossi reported consulting relationships with Merz, DynaMed, and Novartis.

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